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In response to hypersensitivity reactions mediated by antibodies, which are discussed in two anterior divisions, hypersensitivity mediated by T-clitins, also called hypersensitivity of the increased type (HRT) or type IV, they are characterized by immune responses that are initiated mainly by antigen-specific T-clitins. In case of any reaction of hypersensitivity, mediated by antibodies, it is possible to administer a non-immunized individual taken from an immunized or sensitized person. And type IV hypersensitivity reactions can only be done with the help of T-clitin, as shown in animal experiments.
Like in times of hypersensitivity mediated by antibodies, reactions of hypersensitivity mediated by T-clitins, sometimes pathogenic. If activated by contact with an antigen, represented by antigen-presenting cells, reactive T-cells vibrate an unbelievably large number of cytokines, and they can activate other mononuclear cells, but not antigen-specific ones (monocytes and macrophages). This indicates the end pathogenic effect of these reactions.
The main steps to produce before the appearance of such reactions are composed of three stages: 1) activation of antigen-specific Tn1-clitins in a previously sensitized individual; 2) the generation of antigen-specific Tn1-clitins of pro-inflammatory cytokines; 3) radiation and activation of antigen-nonspecific ignition leukocytes. The cycles of the process sound for a long time (24 - 72 years), after which the term hypersensitivity of the improved type appeared. Tsya vіddalenіst hіє є characteristic vіdmіnіstyu GZT vіd reactions mediated іn antibodies, yakі vyyavlyayutsya richly swidshe.
Mal. 16.1. Hypersensitivity reaction of the improved type. In the phase of sensitization by the antigen, the presentation of the APC antigen is observed, which leads to the vilification of cytokines and differentiation of T-clitin in Tn1-clitin. Upon contact with the antigen, the presentation of the APC antigen Tn1-clitin occurs, which leads to the activation of Tn1, the induction of cytokines and the activation of macrophages: MKB - membrane cofactor protein; TNF – swelling necrosis factor
The qi phase is shown in fig. 16.1. The sensitization phase will continue for 1-2 days, at any time, there are some significant mechanisms of T-clitin activation. On the vіdmіnu vіd tsego for zauchennja and activation of such clitin after contact with the antigen in the phase will show approximately 24-72 years - a period that ends with the appearance of histological that clinical signs HRT. Clinical manifestations of HRT in the early stages of the disease, or in some cases, posterigatisya postyno (for example, hypersensitivity of the increased type in case of certain autoimmune diseases).
For an hour, the phases were in contact with the Tn1-clitin antigen and secrete a number of cytokines, especially chemokin and interferon (IFNy), which induce chemotaxis and macrophage activation (Fig. 16.2).
Mal. 16.2. Diagnosis of IFNy on peritoneal macrophages. (A) Normal macrophages in culture; the stench can only begin to stick (before the plastic or the plastic). (B) After IFNy activation, macrophages spread out on the sclera, stretched out to form pseudopodia, and expanded in size (courtesy of Stadecker, Tufts University Medical School)
The activation and activation of antigen-nonspecific clitins by antigen-specific Tn1-clitins is the butt of mutual and congenital immunity, which are discussed in goal. 2. The last cytokine that is secreted by these clitins is IL-12. Vіn ignoring the Tn2 subpopulation and increasing the growth of the Tn1 subpopulation, in this way it leads to an increase in the synthesis of Tn1 cytokines by clitins, which activates macrophages. Also, IL-12 is vitiated by HRT. At the table 16.1 overprotection of the most significant cytokines that take part in the reactions of HRT.
Table 16.1. Cytokines that take part in hypersensitivity reactions of the increased type
The reactions of HRT also take the role of CD8+-T-cells, which are the first to be activated and expand during the sensitization phase of the reaction. Cellin cytokines can irritate tissues through additional mechanisms of cell-mediated cytotoxicity. Activation of CD8+-T-cellin occurs at the link with thyme, which has a rich distribution in the fats of chemical speech and speech, inducing the reaction of DTH and penetrating the cellular membrane (for example, pentadecacatechol - lead to the development of dermatitis caused by contact with broom ivy) ).
The middle cells of the chemical cells react with cytosolic proteins to the approved modified peptides, thus moving into the endoplasmic reticulum, and then on the surface of the cell at the warehouse of MHC molecules of class I. Clitins that present such modified water proteins may choose to avoid CD8+-T-cellins.
Speech, which provokes a reaction, is smeared in oil, which is seen in the leaves of bran ivy or other sporidic growth. Similar olії to avenge catechols (dihydroxyphenols) with high carbohydrate beetle lances. These special features allow speech to penetrate into the skin for the rahunka of lipophilicity (as it allows you to differ in fats, which you can change at the shkirі), as well as covalently for the rahuna of zdatnosti linking with clitin proteins (for example, molecules- noses on the surface of the clitin). Other speeches that are sensitized upon contact also sound like haptens distributed in fats. Different for the chemical form, the stench may have a powerful power to penetrate through the skin and form the conjugated hapten - nose.
Chemical compounds similar to 2,4-dinitrochlorobenzene are used to induce contact sensitization. Practically speaking, in any normal individual, hypersensitivity can appear upon contact with a trial dose of half-heartedness, it is often victorious to assess the scaling of patients to the development of T-cell reactions (cell-mediated immunity ). Various metals, such as nickel and chromium, are present in jewelry embellishments and clasps for lower whiteness, as well as building strength reaction from the side of the scabbard upon contact, simovirno, chelation with whites iri.
It is important that the induction of contact sensitivity is the way of presentation of the causative allergen by Langerhans clitins (APC in shkiri). It is not yet clear whether the sensitizing agent attaches directly to the components of the surface cells of Langerhans, or attaches to the blood serum or tissues, and only then suffocates with these cells.
Mal. 16.3. (A) Contact hypersensitivity type IV reaction - manifestations of a reaction to bran ivy. (B) Type IV contact hypersensitivity reaction - histological pattern of intraepithelial michur and mononuclear infiltrate in the dermis. (B) Shkirna reaction mediated by basophils; basophils and deuces of mononuclear cells 24 years after the introduction of the skin test (these signs are provided with the kind permission of M. Stadecker, Tufts University Medical School)
Cob contact to produce to expand the clones of Tn1-clitin, modern recognition of a specific contact antigen that sensitizes. Further contact with a sensitizing antigen triggers the HRT development phase, as previously indicated. As with this variant of hypersensitivity of the increased type, it is possible to conduct histology, then it is possible to predict the formation of a blister in the epithelium and mononuclear infiltrates in the dermis (Fig. 16.3, B). When this occurs, epidermal clitinitis, spongiosis (flashing intercellular swelling of the epidermis) and michur formation (div. Fig. 16.3, A) occur.
In case of varying moods in the area of primary contact, a sufficient amount of sensitizing antigen is saved. In this way, approximately 1 day, while the expansion of T-clitin is expected, the antigen that has been saved will serve as a provoking factor, and the reaction in the future will be more pronounced. This phase will manifest itself without new contact with a sensitizing antigen.
The most common procedure for testing for the presence of contact sensitivity is a stripe test, in case of a possible antigen, apply on the skin and cover it with a thin bandage. Appearance of a stretch of 3 deb on this dilation of induration and erythema indicates sensitivity to the antigen.
The maximum hour of reaction with granulomas is 21-28 days. Pathological changes are blamed on the absence of macrophages and phagocytosing of pathogens (for example, Mycobacterium leprae) or the splitting of large inert antigens. Granulomas can cause shkidlivy vplivy vplyu zv'yazku z tim, scho stinks zm_shchuyt normal tissue and lead to caseous (cheesy) necrosis. A similar phenomenon is typical for such a contagion, like tuberculosis, M. tuberculosis disease, with which lymphocytes in the ring, the core is removed and significant fibrosis can be suspected.
It is important, however, that different antigens of other microorganisms (such as M. leprae and Leishmania tropica) induce the same tuberculin-type HRT reactions. In this hour of testing for tuberculosis, smash with a route of intraocular injection of a purified lipoprotein extract, seen with M. tuberculosis and called purified protein derivative (PPD).
Mal. 16.4. (A) Hypersensitivity type IV hypersensitivity reaction (tuberculin reaction) is a striking sign that demonstrates the induction of this erythema 48 years after the tuberculin test (courtesy of A. Gottleib, Tulane University Medical School). (B) Hypersensitivity reaction of type IV epilepsy - histological findings demonstrating infiltration of the dermis by mononuclear cells and perivascular muffins (courtesy of M.Stadecker, Tufts University Medical School)
The PPD test (also known as the Mantoux test) is often tested for tuberculosis in the community. Although individuals are already sensitized with antigens of M. tuberculosis as a result of infection with a microorganism, then in the field in the course of 48 - 72 years, it will appear more characteristic of the tuberculin type. The reaction in the appearance of erythema (chervoninnya) and indurations (moving narrowing), which appear after contact, reach a maximum after 72 years (Fig. 16.4, A). It is easy to indulge the induration in the wake of the squealing (squeezing up of the natives) for the day of destruction after the onslaught. These reactions, inspire even more expressions, rarely lead to necrotic ears, and are generally virulent.
A biopsy, broken at an early stage of the reaction, reveals important mononuclear monocyte-macrophage cells with a small number of scattered lymphocytes. It is characteristic that mononuclear infiltrates appear as a perivascular muff before it, as they intensively fill in the place of the antigen (Fig. 16.4, B). Neutrophils are not characteristic participants early stages reactions. Severe tuberculin-type hypersensitivity reactions may progress to granulomatous reactions. Tissue biopsy in such cases reveals a folded picture, which is characterized by the appearance of B-cells and granuloma formation in cases of chronic ear infections. Strengthening of the tissue or induration is explained by the introduction of fibrin in the field of miscarriage.
If you want the PPD test to sound more superficial, in some cases, hybno-negative and hybno-positive reactions increase. In people with compromised immunity (for example, in HIV-infected patients or undergoing intensive chemotherapy), they sometimes show mild-negative reactions to PPD, which is associated with the impossibility of side effects of antigen-specific T-cellin ( anergia).
In these situations, if the test for PPD is victorious for prescribing, if you have previously been exposed to M. Tuberculosis, in people who are vaccinated with non-pathogenic attenuating strains of microorganism, which can cause tuberculosis in thinness (and M. bovis itself - Calmette's bacilli - Guérin (BCG) ) may be responsible for a chibnopositive reaction. The efficacy of the BCG vaccine against legenous tuberculosis in humans is highly variable in different populations.
The main explanations for the importance of viability should be considered in relation to the vaccine and mycobacteria, which are characteristic of specific minds, but the exact mechanism of this dosing is not understood. In some parts of the world, including the United States, BCG vaccination is not universally available due to its cumulative efficacy and significant impact on test results, which should be used to identify if a person was previously infected with M. Tuberculosis.
Studies on guinea pigs have shown that the reaction of the bull of the beast is mediated by T-clitins and is associated with MHC restriction, like the classic reactions, mediated by T-clitins. For the presence of classical HRT, proteo, infiltrates from basophils, it was not suspected. Thus, the skin basophilic hypersensitivity is considered a variant of reactions mediated by T-clitins, but also the exact mechanism of neurodomia. The overarching picture became even more complicated, if it appeared that in some minds a basophilic reaction is a result of a passive transfer of blood serum.
Later basophilic infections were also seen in cases of contact dermatitis caused by allergens, for example, bran ivy, as well as in cases of nirk transplants and with some forms of conjunctivitis. It should be noted that basophils can play a role in certain types of illnesses associated with hypersensitivity to an improved type.
Another application of HRT is the reaction of autoantigens in case of severe autoimmune diseases. As in chronic infections, although they can cause chronic HRT reactions, these reactions are often chronic and result from the activation of autoreactive Tn1-clitin clones. As an example of autoimmune diseases, in the case of increased reactions of hypersensitivity of the increased type, rheumatoid arthritis, type I diabetes and sclerosis can be called.
2. Reactions of hypersensitivity of the mentioned type and mediated by T-clitins are classified by R. Coombs and P. Jell as type IV hypersensitivity.
3. The main steps leading to such reactions are divided into three phases: 1) activation of antigen-specific inflammatory Tn1-clitins in a sensitized individual; 2) inhibition of proinflammatory cytokines (especially IFNy, which activates macrophages) by antigen-specific T-clitins; 3) radiation and activation of antigen-nonspecific ignition leukocytes.
4. Extensive options for HRT, including: 1) contact hypersensitivity, which is characterized by eczema, becomes most pronounced 48-72 years after contact with an allergen; 2) granulomatous hypersensitivity, which is characterized by granulomatous development up to 21-28 dB after contact with antigen; 3) hypersensitivity for the tuberculin type, which is characterized by the appearance of a patch of persistent erythema (blackheads) and induration (moving indentation) with a maximum manifestation after 48 - 72 years after contact. Among other options, there are those who mediate T-cells with autoimmune disease, as well as those who are afraid of after alotransplantation.
5. Cytotoxic CD8+-T-cells may also be involved in the underlying tissue associated with DTH reactions.
6. Phagocytic macrophages are the main histological sign of hypersensitivity of the spontaneous type, and they indicate a chronic effect, even to the point of forming a hypersensitivity pathogen.
7. In depressions, if the macrophages are not immune to the pathogen, the cause is granuloma (granulomatous hypersensitivity). Granulomas can also develop after phagocytosis of inert substances. Histologically, granulomas are characterized by the presence of macrophages, epithelial cells, giant cells, and CD4+ and CD8+ lymphocytes.
R.Koiko, D.Sunshine, E.Benjamini
Related topics "Autoimmune reactions. Hypersensitivity reactions. Transplantation immunity.":Type IV hypersensitivity reactions so call ( HRT). The stench is mindful of cellular immune reactions. In the case of reactions of a negaic type, stench develops not earlier, lower in 24-48 years after the re-introduction of Ag. Development of reactions ( HRT) induce products of microorganism and helminths, natural and non-natural Ag and haptens (faces, cosmetic barniki).
Classic butts hypersensitivity of the increased type (HRT) - tuberculin test and contact dermatitis. Recognition of antigen bound with proteins to the body, immunocompetent cells leads to the activation of T-helper cells, which leads to clonal proliferation of T-effectors HRT. Sensitized lymphocytes secrete cytokines that lure other lymphocytes and macrophages in the middle of an allergic reaction. At the last stages, the reaction is switched on by polymorphonuclear phagocytes, which stimulate the igniter.
Haptens nabuvayut zdatnostі іnіtsіyuvati reactions hypersensitivity of the increased type (HRT) after interaction with high-molecular half-shells, cream with proteins. At their call, the squirrels call out hypersensitivity of the improved type (HRT) in case of triple immunization with small doses in the case of adjuvants. Rich in low molecular weight organic speeches otherwise, inorganic speech (for example, chromium), bonding with the proteins of the skin, play the role of haptens and sensitize the body with trivial contact. As a result, a contact allergy develops, which is clinically manifested by contact dermatitis.
Building with the development hypersensitivity of the increased type (HRT) on different microbial products (for example, anti-tuberculosis, brucellosis) zastosovyt when setting up large samples for the diagnosis of an infectious process, or establishing a possible contact with the body with a viper.
allergic reactions There are two types of response to foreign speech: hypersensitivity of the non-gay type (GNT) and hypersensitivity of the improved type (GST). Prior to HRT, allergic reactions are seen, which appear already after 20-30 minutes after re-exposure with the antigen, and before HRT - reactions, which are blamed not earlier, lower after 24-48 years.
Mechanism and clinical manifestation of HNT and HRT in different ways. HNT is related to the antibody responses, and HRT is associated with cellular reactions.
DZT described above R. Koch (1890). This form is not associated with antibodies, but is mediated by cellular mechanisms for the participation of T-lymphocytes. Before HRT, the following forms of manifestation should be observed: tuberculin reaction, increased allergy to proteins, contact allergy.
On the vіdmіnu vіd reactions I, II and III types Type IV reactions are not associated with antibodies, but are associated with cellular reactions, instead of T-lymphocytes. Reactions of the above type can be caused by sensitization to the body:
1. Microorganisms and microbial antigens (bacterial, fungal, protozoan, viral); 2. Helminths; 3. Natural and piecewise synthesized haptens ( medical care, barvniki); 4. Deyaki squirrels. Also, a reaction of an increased type can be called practically by all antigens. However, it is most clearly manifested by the introduction of polysaccharides, low molecular weight peptides, which are low immunogenic antigens. With this reaction, small doses of antigens are indicated, and even more so with intraocular administration.
Mechanism of allergic reaction this type of activity in the sensitization of T-lymphocyte-helper antigen. Cytotoxicity is also shown by T-lymphocytes themselves. About the role of lymphocytes in the resulting allergic clitinic type to indicate the possibility of transmission of allergies from sensitized organisms unsensitized for additional introduction of lymphocytes, as well as the suppression of reactions for additional antilymphocytic ї orphans.
Morphological picture with allergies of the clitin type, it should be inflammatory in nature, the reaction of lymphocytes and macrophages to the antigen complex, which is approved, with sensitized lymphocytes.
Allergic reactions of the clitin type are manifested in what looks like a tuberculin reaction, increased allergy to protein, contact allergy.
The tuberculin reaction occurs in 5-6 years after the intraocular injection of sensitized tuberculosis creatures or human tuberculin, then antigens in tuberculosis sticks. There is a reaction in the appearance of blackness, swelling, narrowing at the site of introduction of tuberculin. It is accompanied by changes in body temperature, lymphopenia. The development of the reaction reaches a maximum in 24-48 years. The tuberculin reaction is victorious as a diagnostic method for detecting tuberculosis infection or contacting the body with a tubercular wand.
Increased allergy caused by sensitization with small doses of protein antigens with adjuvant, as well as protein conjugates with haptens. In these cases, an allergic reaction occurs not earlier than in 5 days and three days later. Maybe, here the role of increased action of conjugated proteins on lymphoid tissue and sensitization of T-lymphocytes plays a role. Contact allergy causes, as antigens - low molecular weight organic and inorganic speech, which in the body are mixed with proteins, making the conjugates. Conjugated slugs, playing the role of haptens, calling for sensitization. Contact allergy can be blamed on threefold contact chemical speeches, including pharmaceutical preparations, farbs, cosmetic preparations (lipstick, farba for wine). There is a contact allergy in all kinds of dermatitis, that is, damage to the surface balls of the skin.
Value . All reactions of hypersensitivity, In addition, HRT may be of great importance. Your mechanisms to lie down
in the basis of inflammation, which helps to localize the infectious agent or another antigen in the interstices of the tissues and the formation of an overall immune reaction of a chronic nature.
№ 66 Allergic tests, їх daytime, zastosuvannya.
Allergic tests-biological reactions for the diagnosis of low illness, based on increased sensitivity to the body, caused by an allergen.
With various infectious diseases for the activation of the clitinic immunity, the sensitivity of the body to the health of the body and the products of its life develops. On what basis are allergic tests that are vicorated for the diagnosis of bacterial, viral, protozoal infections, mycoses and helminthiasis. Allergic tests may be specific, but sometimes stinks are positive in over-illness and splintering.
Allergic tests are subdivided into two groups-probi in vivoі in vitro.
To the first group(in vivo) there are skin tests that affect the patient indiscriminately and reveal an allergy of negaic (after 20 minutes) and improved (after 24 - 48 years) types.
Allergic testsin vitro based on the revealed sensitization of posture by the body of a sick person. Stop it then, if for some other reason it is not possible to produce blind samples, or in quiet situations, if blind reactions give unclear results. For allergy testing vikoristovuyut allergenic-diagnostic preparations, signs of manifestation of specific sensitization to the body. Infectious allergens, which are vicarious in the diagnosis of infectious diseases, are purified filtrates of broth cultures, or rather suspensions of beaten microorganisms or AG, seen from them.
Try the skins. Infectious allergens should be injected, as a rule, internally or with a brush, rubbing in a scarf in the scarf of the shkir. With the intraocular method, inject 0.1 ml of the allergen into the middle third of the anterior surface with a special thin needle. After 28 - 48 years, evaluate the results of the HRT reaction, depending on the site of the introduction of papule growth.
Non-infectious allergens (pilok roslin, butovy saw, kharchov products, medicinal and chemical preparations) are injected into the skin with a prick (prick-test), with a stripe of scarification and rubbing or rubbing on the inside of the skin with roses rank of allergen. As a negative control, vicorist ІХН, as a positive one - the development of histamine. The results are reversed with a stretch of 20 min (GNT) for the size of the papule (inode up to 20 mm in diameter), the presence of a streak and a stinger. Intra-shnyoshkirnі try to put at times negative chi sumnіvny result prick-test. Alternately with the rest, the dose of the allergen is changed at 100-5000 times.
Screening tests for the presence of HRT are widely used to detect infection in people with mycobacterium tuberculosis (Mantoux test), brucellosis (Burne test), leprosy (Mitsudi reaction), tularemia, glanders, actinomycosis, dermatomycosis, toxoplasmosis , active gel.
Probyin vitro .Tsі methodi doslіdzhennya bezpechnі for the sick, dosit sensible, allow kіlіkіsno assess the level of allergy to the body.
In this hour, tests have been developed for the determination of sensitization, which are based on reactions T- and B-lymphocytes, tissue basophils, revealed upper specific IgE in blood sirovattsі and in. Before them, one can see the reactions of galvanization of migration
leukocytes and blast transformation of lymphocytes, specific rosette formation, Shelley basophil test, degranulation reaction of tissue basophils, as well as allergosorbent methods (designation of specific IgE in blood sirovats). The reaction of galvanic migration of leukocytes (RTML). RTML is based on suffocated migration of monocytes and other leukocytes under the influence of mediators, which are sensitized by lymphocytes, in the presence of a specific allergen.
Reaction of blast transformation of lymphocytes (RBT). The basis of this reaction is the ability of normal lymphocytes in peripheral blood to enter mitosis and transform into blast forms during cultivation in vitro pіd dієyu specific factors - allergens and nonspecific stimulant in mitogenesis - mitogens (phytohemagglutinin, concanavalin A, lipopolysaccharides and other speech).
The reaction of a specific rosette. Rosettes are characteristic solutions that blame in vitro afterward, the adhesion of erythrocytes to the surface of immunocompetent cells. Rosette formation can occur spontaneously, shards of T-lymphocytes from humans can reach receptors to sheep erythrocytes. Spontaneous rosette of healthy people become 52 - 53% and є an indicator of the functional state of T-lymphocytes. This phenomenon is also observed in that case, as vicarious erythrocytes, on some fixation of allergic reactions.
Degranulation reaction of tissue basophils. The technique is based on the fact that in case of an allergen, degranulation of tissue basophils of the scura, anteriorly sensitized by cytophilic AT from the blood serum of a sick person, is observed.
Shelly's basophil test. Apparently, the basophilic granulocytes of humans and rabbits are also degranulated in the presence of a sickly and allergen serosa, to the point of being a sensitive patient.
Designated antitil class IgEinvitro. Laboratory diagnostics of illnesses, which are based on GNT,
based on designated allergen-specificIgEanti-IgE. In case of vicarious radioactive label, the method is called the radioallergosorbent test (PACT), and more often, as a vicarious label, the enzyme or fluorescent speech (FAST) is used. Hour of analysis - 6 - 7 years. The principle of the method: fixing on a solid basis, the allergen is incubated from the blood serum of the sick; change at the syrovattsі specific IgEanti-IgE are associated with an allergen and, in such a rank, are fixed on the basis of and can enter into a specific relationship with the indications that they are given. anti-IgE.
№ 67 Hypersensitivity of the Negative type. Vindication mechanisms, clinical significance.
Hypersensitivity of the Negative type(HNT) - hypersensitivity, stimulated by antibodies (IgE, IgG, IgM) against allergens. It develops through a sprat of whilin or a year after the allergen develops: judges expand, their penetration increases, swollen, bronchospasm, hanging, swelling develop. The late phase of HNT is supplemented by the production of eosinophil and neutrophil products.
Before GNT, there are I, II and III types of allergic reactions (according to Gell and Coombs): Type II - cytotoxic, sensing of IgG, IgM; Type III - immunocomplex, which develops when the immune complex of IgG, IgM with antigens is established. In the okremium type, antireceptor reactions are seen.
Main types of hypersensitivity reactions
Type I - anaphylactic. Upon initial contact with the antigen, IgE is uti- lized, which attaches the Fc-fragment to smooth cells and basophils. Repeated injections of the antigen cross-link with IgE on cells, causing degranulation, histamine and other mediators of allergy.
The primary intake of the allergen causes the production of IgE, IgG4 by plasma cells. Synthesis of IgE is attached by an Fc-fragment to Fc-pe ceptors (FceRl) of basophils in blood and dangerous cells in mucous membranes, healthy tissue. In case of repeated exposure to the allergen on dangerous clitins and basophils, IgE complexes with the allergen are established (cross-linking with FceRl antigen), which results in degranulation of clitins.
Clinical manifestations of type I hypersensitivity.
Clinical manifestations of type I hypersensitivity may progress to atopy aphids. Atopia- Falling-off to the development of HNT, due to the increase in the conversion of IgE antibodies to an allergen, the increase in the number of Fc-receptors for cich antibodies on dangerous cells, the peculiarities of roses under the dangerous cells and increased penetration of tissue bars єрів.
Anaphylactic shock- flows sharply with a development of collapse, swearing, spasm of smooth muscles; often ends death. Kropivnitsa- The penetration of ships increases, the skin of red ones, bulbs, sverbіzh appear. Bronchial asthma
Inflammation, bronchospasm develop, secretion of mucus in the bronchi becomes stronger.
Type II - cytotoxic. Antigen, spread on cells, "recognized" by antibodies of the IgG, IgM classes. In the case of interaction of the “clitin-antigen-antibody” type, activation of the complement and the disruption of the cells after the trioma directly occurs: complement-depositing cytolysis; phagocytosis; anti-body cell cytotoxicity. Hour of reaction - hvilin abogodinnik.
Prior to type II hypersensitivity, there are close antireceptor reactions (so called type IV hypersensitivity), the basis of which are anti-receptor antibodies, for example, anti-receptor antibodies to hormones.
Clinical manifestation of type II. According to type II hypersensitivity, deuces of autoimmune ailments develop, conditioned by the appearance of autoantibodies to antigens in the body tissues: malignant myasthenia, autoimmune hemolytic anemia, puffiness vulgaris, Goodpasture's syndrome, autoimmune hyperthermia thyroidism, insu. Autoimmune hemolytic anemia call out antibodies against Rh-antigen of erythrocytes; erythrocytes collapse into after complement activation and phagocytosis. drug-induced hemolytic anemia, granulocytopenia and
thrombocytopenia are accompanied by the appearance of antibodies against drugs - hapten and cytolysis of clitin, what to revenge Antigen.
Type III - immunocomplex. Antibodies of the class IgG, IgM are produced from various antigens of the immune complex, thus activating the complement. When there is an excess of antigens or lack of complement, immune complexes are deposited on the walls of the vessels, basement membranes, such structures that Fc receptors detect.
The primary components of type III hypersensitivity and variant immune complexes are antigen-antibody and complement (anaphylatoxins C4a, C3a, C5a). When there is an excess of antigens and lack of complement, the immune complexes are deposited in the walls of the vessels, basement membranes, tobto. structures that can detect Fc receptors. Ushkodzhennya is saturated with platelets, neutrophils, immune complexes, complement. Pro-inflammatory cytokines are seen, including TNF-α and chemokines. At the last stages, before the process, macrophages appear.
The reaction is the bouty of the nitrous (set, Sirovatkov brushwood), the abundance of the frog organ, tissue, including the shkiru (set, the system of erytemetrosy Vovchak, the reacts of Artyus), nirki (linked, excaval jade), legendary (lifting, aspergilosis) abstracts. This reaction may be influenced by a variety of microorganisms. It develops in 3-10 years after exposure to the antigen, like in the Arthus reaction. The antigen can be exogenous (chronic bacterial, viral, fungal, or protozoan infections) or endogenous, as in systemic erythematous canine. Clinical manifestation III type.Sirovatkov's ailment vіdbuvaєtsya with the introduction of high doses of the antigen, for example, the Kіnsk protipravtsevoї sirovatka. After 6-7 days, antibodies against anti-Kinsk protein appear in the blood, which, in conjunction with this antigen, establish immune complexes, which are found in the walls of blood vessels and tissues. Developing systemic vasculitis, arthritis (complexes in marrows), nephritis (complexes in nirks).
Arthus reaction develops with repeated intraocular injection of antigen, which locally approves immune complexes with antibodies that accumulated earlier. It appears in a blur, hemorrhagic inflammation and necrosis.
№ 68 Anaphylactic shock and syrovatkova ailment. Cause blame. Mechanism. Їхнє preperedzhennya.
Anaphylaxis is a reaction of a negaine type, which is due to parenteral repeated administration of an antigen in case of a severe antigen-antibody complex and is characterized by a stereotypical clinical and morphological picture.
The main role in anaphylaxis is played by cytotropic IgE, which can be sporadic to clitin, zocrema basophils and dangerous clitin. After the first contact of the organism with the antigen, IgE is absorbed, which, after cytotropy, is adsorbed on the surface of other clitins. When re-entering the body of the IgE antigen, the antigen binds to the IgE-antigen complex on the cellular membrane. The complex of poshkodzhuє kіtiny, yakі vіdpovіd on tse see mediators - histamine and histamine-like speech (serotonin, kinіn). Ci mediators are connected by receptors, which are on the surface of functional mucosal, secretory, mucosal and other clitins, inducing active reactions. It leads to shortening of the smooth muscles of the bronchi, intestines, sich michur, increased penetration of the vessels and other functional and morphological changes that are accompanied by a clinical manifestation. Clinically, anaphylaxis is manifested in the appearance of a backside, poison, weakness, restlessness, trial, mimicry, defecation and other. The anaphylactic reaction proceeds in three phases: in the 1st phase, the antigen-antibody reaction itself occurs; in the 2nd phase, mediators of anaphylactic reactions are seen; in the 3rd phase, functional changes are manifested. Anaphylactic reaction vinikaє through a sprat of whilin or a year after the re-introduction of the antigen. The intensity of the reaction to lie down depending on the dose of the antigen, the number of antibodies that are approved, the type of creature and may end in death or death. Anaphylaxis can easily be elicited in animal experiments. The optimal model for the implementation of anaphylaxis is guinea pig. Anaphylaxis can be blamed on the introduction of any antigen in any way (through a dical path, a herbal tract) for the mind that the antigen calls for the introduction of immunoglobulins. The dose of an antigen that leads to sensitization, to increase sensitivity, is called sensitization. It sounds too small, the shards of large doses can cause sensitization, and the development of an immune infection. The dose of the antigen, introduced already sensitized to her creatures and which elicits manifestation of anaphylaxis, is called divided. The allowable dose is guilty but significantly larger, lower sensitizing.
Stan sensitization after sensitization with antigen saved for months, sometimes; The intensity of sensitization can be individually changed by introducing small doses of the antigen, which induces and removes part of the antibodies from circulation in the body. This principle was vikoristano for desensitization (hyposensitization), tobto. prevention of anaphylactic shock with re-introduction of the antigen. Formerly, the method of desensitization was propagated by the Russian teachings of A. Bezredk (1907), which is called the method of Bezredka. The method is based on the fact that people had previously withdrawn any antigenic drug (vaccine, serum, antibiotics, blood preparations and others), with repeated administration (due to the presence of a new sensitivity to the drug), a small dose (0.01; 0.1 ml), and then, after 1-1 "/ 2 years, - the main one. This method is used in all clinics for the development of anaphylactic shock; this method is obov'yazkovim.
Possible passive transfer of anaphylaxis with antibodies.
Sirovatkovoy ailment name the reaction what is to be blamed for a single parenteral administration of large doses
syrovatkovyh and other protein preparations. Sound the reaction winikaє in 10-15 deb. Mechanism of syrovatkovoj ailment of apposition with the adoption of antibodies against the introduced foreign protein (antigen) and severe attack on the cells of antigen-antibody complexes. Clinically, syrovatkova ailment is manifested by swollen skin and mucous membranes, increased body temperature, swollen loam, hanging and stinging skin; changes in the blood are suspected (improved SOE, leukocytosis and others). The terms will show that heaviness
syrovatkovy ailment to lie in the presence of circulating antibodies and doses of the drug. This is explained by the fact that on the 2nd day after the introduction of white blood cells, antibodies are vibrated to white blood cells and the antigen-antibody complex is established. Prevention of syrovatkovo ailment is based on the method of Bezridka.
№ 70 Features of antiviral, antibacterial, antifungal, antitumor, transplant immunity.
Antivirus immunity. The basis of antiviral immunity is cellular immunity. Anti-virus antibodies to the health neutralize only pozaklitinno roztashovanі vіrusi, as a factor in non-specific immunity
Sirovatkovy anti-rusny ingibіtori. Such viruses, honed and blocked by proteins to the body, are purged by phagocytes, or they are removed from the section, then that. (the so-called "vidilniy immunitet"). Interferons exert antiviral resistance, inducing the synthesis of enzymes in clitins, which inhibit the production of nucleic acids and proteins of viruses. The cream of this, interferon, may have an immunomodulatory effect, increase the expression of antigens in the head histosum complex (MHC) in clitins. Antiviral defense of the mucous membranes of the brain with secretory IgA, which, in conjunction with viruses, alters their adhesion to epitheliocytes.
Antibacterial immunity directing both against bacteria and against toxins (antitoxic immunity). Bacteria and their toxins are neutralized by antibacterial and antitoxic antibodies. Bacteria (antigen)-antibody complexes activate complement, the components of which are attached to the Fc-fragment of the antibody, and then establish a membrane attack complex, which destroys the outer membrane of the cellular wall of gram-negative bacteria. Peptidoglycan of cell walls of bacteria is destroyed by lysozyme. Antibodies and complement (C3b) envelop bacteria and “glue” them to Fc- and C3b receptors of phagocytes, playing the role of opsonins together with other proteins, which enhance phagocytosis (C-reactive protein, fibrinogen, mannan zuval lectin).
The main mechanism of antibacterial immunity is phagocytosis. Phagocytes directly move to the object of phagocytosis, reacting to chemoattractants: microbial speech, activated complement components (C5a, C3a) and cytokines. Antibacterial infection of mucous membranes with secretory IgA, which, in conjunction with bacteria, alters their adhesion to epitheliocytes.
Antifungal immunity. Antibodies (IgM, IgG) are detected in low titers in mycoses. The basis of antifungal immunity is cellular immunity. In tissues, phagocytosis occurs, an epithelioid granulomatous reaction develops, and sometimes thrombosis of blood vessels. Mycoses, especially opportunistic, often develop after trial antibacterial therapy and in immunodeficiencies. The stench is accompanied by a rise in hypersensitivity of the improved type. A possible development of allergic diseases after respiratory sensitization by fragments of mind-pathogenic fungi canopies of Aspergillus, Penicillium, Mucor, Fusarium and in.
Anti-swelling immunity grounds for Th1-deposit cellular immune response, which activates cytotoxic T-lymphocytes, macrophages and NK-cells. The role of the humoral (antile) immune response is small, the antibody shards, linked to antigenic determinants on chubby cells, screen for their types of cytopathogenic immune lymphocytes. Fluffy antigen is recognized by antigen-presenting clitins (dendritic clitins and macrophages) and without intermediary or through T-helper (Th1) is presented to cytotoxic T-lymphocytes, which destroy the plump clitin-target.
The cream of specific anti-tumor immunity, immune surveillance of the normal warehouse of tissues is realized due to non-specific factors. Non-specific factors that stimulate puffer cells: 1) NK-cells, a system of mononuclear cells, the antitumor activity of which is enhanced by the influx of interleukin-2 (IL-2) and α-, β-interferons; 2) LAK cells (mononuclear cells and NK cells activated by IL-2); 3) cytokines (α - and β - interferon, FNP-α and IL-2).
Transplant immunity name an immune reaction to a macroorganism directed against a transplanted foreign foreign tissue (graft). Knowledge of the mechanisms of transplantation immunity is a necessary solution to one of the most important problems of modern medicine - transplantation of organs of the prosecutor's office and tissues. A good report showing that the success of the operation for the transplantation of foreign organs and tissues in the most important cases is due to the immunological integrity of the tissues of the donor and the recipient.
The immune reaction to foreign cells and tissues is due to the fact that antigens that are genetically foreign to the body are in their warehouse. Qi antigens, which took away the name of transplantation or antigens in histosummity, are the most frequently presented on CPM clitin.
There is no reaction in the case of the totality of the donor and the recipient in terms of histosummancy antigens - it is also possible only for identical twins. The diversity of the reaction to the invasion is rich in what to lie down at the stage of foreignness, to the material that is transplanted, and I will become the recipient's immunoreactivity.
Upon contact with foreign transplantation antigens, the body reacts with cellular and humoral immunity factors. The main factor in cellular transplant immunity is T-killer. Cells after sensitization by donor antigens migrate to the graft tissue and induce anti-cellin-mediated cytotoxicity on them.
Specific antibodies that bind to foreign antigens (hemagglutinins, hemolysins, leukotoxins, cytotoxins) may be important in the formation of transplantation immunity. They trigger anti-body mediation of cytolysis to the graft (complement mediation and anti-body cell mediated cytotoxicity).
Possibly adaptive transfer of transplantation immunity for additionally activated lymphocytes or specific anti-irritant in a sensitized individual of an intact macroorganism.
The mechanism of immune suppression of transplantation of cells and tissues may have two phases. In the first phase, near the graft, that vessel is prone to accumulation of immunocompetent cells (lymphoid infiltration), including T-killers. In the other phase, destruction of cellular graft by T-killers is observed, macrophage lanka, natural killer, and specific anti-thylogenesis are activated. Blame the immune inflammation, thrombosis of the blood vessels, disruption of the graft ingestion and death. Ruined tissues are utilized by phagocytes.
In the process of the reaction, a clone of T-B-cellin of the immune memory is formed. A repeated test of transplantation of these organs themselves and tissues reveals a second immune response, as it flows more gurglingly and quickly ends in transplant rejection.
From the clinical point, the lesion is seen as hot, overheated and overstretched graft. The stench is roiled by the hour of the implementation of the reaction and the other mechanisms.
№ 71 Concepts of clinical immunology. Immune status of a person is the factor that is poured into her.
Clinical Immunology-the same clinical laboratory discipline that deals with the development of nutrition, diagnostics and the treatment of ailments with various diseases and pathological states, which are based on immunological mechanisms, as well as states, in therapy and prevention of such immunological preparations play a leading role.
Immune status-ce structural and functional state of the immune system of the individual, which is characterized by a complex of clinical and laboratory immunological indications.
In this way, the immune status characterizes the anatomical and functional state of the immune system, so that it is up to the immune response to the song antigen at a given moment.
For immune status add such factors:
Climato-geographical; social; ecological (physical, chemical and biological); "medical" (infusion of medical speeches, operational delivery, stress toshko. bud.).
Middle of climatic and geographical factors the immune status is influenced by temperature, moisture content, somnolent radiation, daylight hours, etc. For example, phagocytic reaction and high allergic tests are less pronounced in residents of prairie regions, lower in residents of the prairie. Epstein-Barr virus in people of white race causing infectious disease - mononucleosis, in people of black race - oncopathology (Burkitt's lymphoma), and in people of yellow race - other oncopathology (nasopharyngeal carcinoma) a), moreover, it is less for people. Inhabitants of Africa are less likely to fall ill with diphtheria, lower European population.
To social factors, what to add to the immune status, eat food, lively-pobutovі mind, professional shkidlivosti meagerly. Important value can be balanced and rationally eaten, shards of speech, necessary for the synthesis of immunoglobulins, for inducing immunocompetent cells and their functioning. It is especially important that the diet contains essential amino acids and vitamins, especially A and C.
Significant impact on the immune status of the body is given to the living-pobutovі mind. Living in filthy living minds leads to a decrease in the overall physiological reactivity of immunoreactivity, which is often accompanied by an increase in infectious disease.
The great impact on the immune status is given by professional shkidlivosti, the shards of a person spend a significant part of their life on a robot. To virobnicheskikh factors, yakі can put an unacceptable infusion on the body and reduce immunoreactivity, introduce ionizing radiation, chemical speech, microbial and life products, temperature, noise, vibration, etc. industry (energy, gyrnichochemical, aerospace and other). Salts of important metals, aromatics, alkyl compounds and other chemicals can be unfriendly to the immune status, including microbes, disinfectants, pesticides, otrutochemicals, which are widely used in practice. Such a professional shkіdlіvіst skhilnі pratsivniki khіmіchnyh, naftokhіmіchnyh, metallurgical izvobnitstv and іnshih.
Microbes and products of their vitality (mostly proteins and iodine complexes) in biotechnological chemists, as well as antibiotics, vaccines, enzymes, hormones, feed bio lka and others.
Such factors, such as low or high temperature, noise, vibration, lack of light, can reduce immunoreactivity, relying on the mediation of the immune system through the nervous and endocrine systems, as a result of a close relationship with them unno system.
Global impact on the immune status of people is put on environmental factors, in Persh Cherga, the pollution of the middle ground with radioactive speeches (in the case of radioactive waste from nuclear reactors, the release of radionuclides from reactors in case of accidents), the widespread infestation of pesticides in the country's state of power, and the spread of chemical pesticides facilities and vehicles, biotechnological productions.
Various diagnostic and medical manipulations are added to the immune status. , likarska te-
rapia, stress . Unprimed and often blocked radiography, radioisotope scanning can be added to
immune system Immunoreactivity changes after injuries and surgical operations. A lot of medicinal preparations, including antibiotics, can be used as an immunosuppressive drug, especially in case of trivial administration. Stress destroys the robotic T-system of the immune system, pushing us forward through the central nervous system.
№ 72 Evaluation of the immune status: the main indicators and methods of their identification.
Irrespective of the variability of immunological indications in the norm, the immune status can be determined by the way of setting a complex of laboratory tests, which include the assessment of the factor of nonspecific resistance, humoral (B-system) and cellular (T-system) immunity.
Assessment of the immune status be carried out in clinics for transplantation of organs and tissues, autoimmune diseases, allergies, for the detection of immunological deficiency in various infectious diseases somatic illnesses to control the effectiveness of treatment of ailments associated with impaired immune systems. Depending on the capabilities of the laboratory, the assessment of the immune status is most often based on the designated complex of offensive indications:
zagalny clinical obstezhennya;
camp factors of natural resistance;
humoral immunity;
clitin immunity;
additional tests.
With severe clinical obstezhennі care for the patient's scars, anamnesis, clinical symptoms, the results of a global blood test (including the absolute number of lymphocytes), data on biochemical follow-up.
Humoral immunity indicative of the level of immunoglobulin classes G, M, A, D, E in blood serum levels, the number of specific antibodies, immunoglobulin catabolism, non-gain type hypersensitivity, indication of B-lymphocytes in peripheral blood, B-l blast transformation imfocytiv subdivision B-clitin.
Stan clitinnogo іmunіtetu evaluate for the number of T-lymphocytes, as well as subpopulations of T-lymphocytes in peripheral blood, blast transformation of T-lymphocytes in the presence of T-cell mitogens, hormones in the thymus, the level of secretion of cytokines, as well as staging screen samples with allergens, contact sensitivity. For the setting of high-level allergic tests, antigens are used, which in the norm may be sensitized, for example, the Mantoux test with tuberculin. Health to the body before the induction of primary immune response can give contact sensitization with dinitrochlorobenzene.
How dodatkovі tests to assess the immune status, it is possible to test such tests, as the designation of bactericidal blood serum, titration of C3-, C4-components in complement, designation together C-reactive protein in blood sputum, rheumatoid factors and other autoantibodies.
Such a rank assessment of the immune status is carried out on the basis of setting a large number of laboratory tests, which allow assessing the state of both the humoral and cellular parameters of the immune system, as well as factors of nonspecific resistance. All tests were divided into two groups: tests of the 1st and 2nd level. Tests of the 1st level can be tested at the first clinical immunological laboratory of primary health care, they are used for the primary manifestation of symptoms with a clearly expressed immunopathology. For accurate diagnosis, tests of the 2nd level are victorious.
№ 73 Disorders of the immune system: primary and secondary immunodeficiencies.
Immunodeficiency-destruction of the normal immune status, caused by a defect in one or more mechanisms of immune response.
Separate primary, or congenital (genetic), and secondary, or onset, immunodeficiency.
Primary, congenital, immunodeficiencies.
As the primary immunodeficiency is seen in such a way, with any impaired immune humoral and clitinic mechanisms associated with a genetic block, it is genetically conditioned to the undetectable organism to implement that foreign immunological reagent news. Disorders of the immune system can develop as the main specific lanka in the functioning of the immune system, and officials that signify nonspecific resistance. Possible combinations and selective variants of immune disorders. Depending on the nature of the damage, there are differences in humoral, clitin, and combination immunodeficiency.
Congenital immunodeficiency syndromes and illnesses are a rare manifestation. Causes of congenital immunodeficiencies can be a subset of chromosomes, point mutations, enzyme defects in the exchange of nucleic acids, genetically damaged membranes, damage to the genome in the embryonic period, and so on. As a rule, primary immunodeficiency manifests itself in the early stages of the postnatal period and in the early stages of the postnatal period and in the early stages of the postnatal period. Primary immunodeficiencies may appear in phagocytosis deficiency, complement system, humoral immunity (B-system), cellular immunity (T-system) or in combined immunological deficiency.
Secondary, or on the other hand, immunodeficiency
Secondary immunodeficiencies in the form of primary immunodeficiencies develop in the immune system, which normally functioned in the people. The stench is molded under the infusion dovkilla on a par with the phenotype and the damage to the impaired function of the immune system due to various illnesses or unacceptable impacts on the body. In case of secondary immunodeficiencies, T-I B-system immunity can be affected, factors of nonspecific resistance can also be affected. The side effects of immunodeficiency are significantly more frequent, less primary. Secondary immunodeficiencies, as a rule, subside and undergo immunocorrection, thus restoring the normal activity of the immune system.
Secondary immunodeficiencies can be: after past infections (especially viral ones) and invasions (protozoan and helminthiasis); with opikovy ailment; with uremia; with puffiness; when the exchange of speeches and vysnazhenni is damaged; with dysbiosis; with severe injuries, major surgical operations, which are especially conducive to severe anesthesia; at prominenny, dії khіmіchnyh rechovina; in case of old, as well as medicamentous, applied from taking drugs.
For an hour they see guilt antenatal(for example, non-falling forms of the DiGeorge syndrome), perinatal(for example, neutropenia of the newborn, viklikana maternal sensitization to neutrophil antigens fetus) that postnatal secondary immunodeficiency.
Behind the clinical break you see compensated subcompensatedі decompensated forms of secondary immunodeficiencies. The compensated form is accompanied by an increased susceptibility to the organism to infectious agents, which are called opportunistic infections. The subcompensated form is characterized by scaling up to chronic infection processes. The decompensated form manifests itself in generalized infections caused by mentally pathogenic microbes (UPM) and evil neoplasms.
Vіdomy subdivided secondary immunodeficiencies to:
Physiological, neonatal, pubertal period, vagility and lactation, old age, biorhythmicity, ecological, seasonal, endogenous intoxication, radiation, HF, pathological, post-infection, stress, regulatory-metabolism chni, medicamental, oncological.
Immunodeficiencies, both primary and especially secondary, widely spread among people. The stench is the reason for the manifestation of many ailments and pathological conditions, which requires prevention and treatment for the help of immunotropic drugs.
№ 74 Agglutination reaction. Components, mechanism, methods of setting. Zastosuvannya.
Agglutination reaction- It is easy to set up a reaction, when it is connected with antibodies of corpuscular antigens (bacteria, erythrocytes or other cells, inorganic particles with antigens adsorbed on them, as well as macromolecular aggregates). It leaks due to the presence of electrolytes, for example, when adding an isotonic solution to sodium chloride.
zastosovitsya different variants of the reaction of agglutination: flared, oriental, indirect and in. RA vicory for:
detection of antibodies in blood syrovirus diseases, for example, in brucellosis (reaction of Wright, Heddelson), typhoid fever and paratyphoid fever (reaction of Vidal) and other infectious diseases;
the appointment of a health worker, seen as sick;
identification of blood groups for vicarious monoclonal antibodies against allo-antigens of erythrocytes
For vyznachennya in ailing antibodies set a fired agglutination reaction: Before breeding the blood serosa of the sick, add a diagnosticum (a suspension of killed microbes) and after a few years of incubation at 37 ˚С, the most brood of the sirovatka (titre of the sirovatka) is indicated, when agglutination is established, then the siege is established.
The nature and speed of agglutination lie in the form of antigen and antibodies. An example is the peculiarity of the interdependence of diagnosticums (O and H-antigens) with specific antibodies. The reaction of agglutination with O-diagnosticum (bacteria, beaten with heat, which saved the heat-stable O-antigen) is seen in the appearance of fine-grained agglutination. The reaction of agglutination with H-diagnosticum (bacteria, beaten with formalin, which saved the heat-labile flagellar H-antigen) is great and protracted.
It is necessary to appoint an alarm clock, visions of the sick, to set orienting reaction of agglutination, zastosovuyuchi diagnostic antibodies (agglutination sirovatka) to carry out serotyping of the bug. Orientation reaction should be carried out on a slide. To a drop of diagnostic agglutinating sirowort in breeding 1:10 or 1:20, add a pure culture of the vigilante, seen in the sick. Instructed to put the control: the deputy of the sirovatka to apply a drop of sodium chloride. When a layer-like sediment appears in drops with sirovatka and microbes, set up an agglutination reaction in test tubes with agglutinated sirovatka, which increases, to add 2-3 drops of suspension of sprout to them. Agglutination is paid for the siege and the stage of enlightenment of the native land. The reaction is considered to be positive, as agglutination is indicated in bred, close to the titer of diagnostic serum. At the same time, guard the control: sirovatka, bred with an isotonic solution of sodium chloride, is guilty of buti prozora, the dependence of microbes in the same variant is equally calamous, without siege.
Various disputed bacteria can be agglutinated by one and the same diagnostic agglutinating sirovatka, which makes it easier to identify them. Therefore, they are coryzed by adsorbing agglutinating siroworts, which have been seen to cross-react antibodies with adsorption pathways of their native bacteria. In such sirovatkah, antibodies are saved that are less specific to bacteria.
№ 75 Coombs reaction. Mechanism. components. Zastosuvannya.
The agglutination reaction for the designation of anti-Rh antibodies (indirect Coombs reaction) is stopped in patients with intravascular hemolysis. Some ailments show anti-Rhesus antibodies, which are incomprehensible, monovalent. The stench specifically interacts with Rh-positive erythrocytes, but does not call for their agglutination. The presence of such non-obvious antibodies is indicative of the indirect Coombs reaction. For this, anti-Rhesus antibodies + Rh-positive erythrocytes are supplemented with antiglobulin serum (antibodies against human immunoglobulins), which causes agglutination of erythrocytes. For additional Coombs reaction, pathological conditions are diagnosed, associated with intravascular lysis of erythrocytes of immune origin, for example, hemolytic ailment of newborns: erythrocytes of a Rh-positive fetus are associated with circulating in the blood with incompetent antibodies to the Rh factor, they crossed over the Rh factor.
mechanism The folding nature of the manifestation of non-identical (monovalent) antibodies is due to the fact that these antibodies, binding to septopes of a specific antigen, do not establish the structure of the lattice and the reaction between antigens and antibodies do not show agglutination, no precipitation, no other tests. For the manifestation of complexes that have settled, the antigen is an antibody
be brought to vikoristovuvaty dodatkovі test systems. For the detection of incompetent antibodies, for example, to the Rhesus antigen of erythrocytes in the erythrocyte blood serosa, the reaction should be carried out in two stages: 37 ° With a stretch; 2) until recently after the first stage of erythrocytes, give the rabbit an anti-human anti-globulin serum (in advance of the titrated robotic breeding). After incubation stretching 30 min. at 37 ° C, the results are evaluated for the presence of hemagglutination (positive reaction). It is necessary to control the ingredients of the reaction: 1) antiglobulin serum + sensitization with specific erythrocyte antibodies; 2) normal erythrocytes + antiglobulin erythrocytes; 3) enriched with dosledzhuvanny sirovatka Rh-negative erythrocytes + antiglobulin sirovatka.
№ 76 Reaction of passive hemagglutination. components. Zastosuvannya.
Reaction of indirect (passive) hemagglutination (RNHA, RPHA) based on vicarious erythrocytes (or latex)
adsorption on their surface by antigens or antibodies, the interaction of these with other antibodies or antigens of the blood serosa of ailments leads to gluing and falling of erythrocytes to the bottom of the test tube or clots at a scalloped siege.
components. For the production of RNGA, erythrocytes of sheep, horse, rabbit, chicken, mouse, humans and others can be harvested in reserve, treated with formalin or glutaraldehyde. The adsorption capacity of erythrocytes increases when testing with tannin or chromium chloride.
Antigens in RNHA can be polysaccharide antigens of microorganism, extracts of bacterial vaccines, antigens of viruses and rickets, as well as other speech.
Erythrocytes, sensitized by arterial hypertension, are called erythrocyte diagnosticums. For the preparation of erythrocyte diagnosticum, vicorous erythrocytes of a sheep are most often used, as they may have a highly adsorbing activity.
Zastosuvannya.RNGA is used for the diagnosis of infectious ailments, for the determination of gonadotropic hormone in the section with established vaginess, for the manifestation of increased sensitivity to medicinal preparations, hormones and in other cases.
mechanism.Reaction of indirect hemagglutination (RIHA) is significantly more sensitive and specific, lower reaction of agglutination. Її vykoristovuyut for іdentifikatsії zabudnik for yogo antigenic structure or for indication and іdentifikatsії bacterial produktіnі - ksіnіv v dolіdzhuvanym pathologicheskiy materialі. Vydpovidno vikoristovuyut standard (commercial) erythrocyte anti-diagnostic, otrimani adsorption of specific antibodies on the surface of tannins (tannin-treated) erythrocytes. At the wells of plastic plates, a subsequent development of the final material is prepared. Then add the same 3% suspension of erythrocyte antibodies to the well in the skin hole. If necessary, the reaction should be placed in parallel with a number of rows of wells with erythrocytes, with antibodies of different group specificity.
After 2 years of incubation at 37 °C, check the results, evaluating old look sedimentation of erythrocytes (without streaking): in case of a negative reaction, sedimentation appears at the appearance of a compact disk or a ring on the bottom of the hole, with a positive reaction - a characteristic fine sedimentation of erythrocytes, a thin layer with uneven edges.
№ 77 Reaction of coagglutination. Mechanism, components. Zastosuvannya.
Coagglutination reaction zastosovuyt for the appointment of antigens for additional antibodies, adsorbed on the protein A of staphylococcus aureus (diagnosticum antigen).
Bilok A there may be spores to the Fc-fragment of immunoglobulins, that is, bacteria that have been developed by the immunological diagnostic shrimp, non-specifically adsorb shrimp antibodies, and then interact with the active centers of the sick. As a result of coagglutination, plastics are formed, which are composed of staphylococci, antibodies of the diagnostic sirowort and an intoxicated microbe.
mechanism Evidence that protein A, which is found on the surface of Staphylococcus aureus, selectively reacts with the Fc fragment of IgGl, G2, G4, overwhelms the free antideterminants of Ab, yak, interacting with homologous Ag, causes agglutination of staphylococci OKIV. For setting COA, zastosovuyut commercial staphylococcal reagents, which are placed in ampoules or dried in the wells of polystyrene plates or a subject storage. To the reagent, add 0.01-0.1 ml of an additional culture of aborosinous Ag, incubate at room temperature 10-30 minutes (for the minds of setting the reaction on the face) or 18-20 years (with the minds of setting the reaction in capillaries). The appearance is carried out in the same way, as in case of primary RA. Agglutination is paid for the siege and the stage of enlightenment of the native land. The reaction is considered to be positive, as agglutination is indicated in bred, close to the titer of diagnostic serum. Watch out for the controls at once: sirovatka, diluted with isotonic sodium chloride, due to prozor, dependence of microbes on the same variant
Postupovo kalamutnoy, without a siege.
№ 78 Reaction of galvanization of hemagglutination. Mechanism. components. Zastosuvannya.
Hemagglutination galvanization reaction(RTGA)-method of іndifіkatsya viyavannnia vi-Russian antitrus in Sirovatzi of blood, falling on the phenomena of the verticitiv with the drug, and the virus, in the present, in the nye sirovatka blood.
Hemagglutination galvanization reaction (RTGA) based on the blockade, smothered antigens of viruses with antibodies of the immune serosa, after which the viruses exercise power to agglutinate erythrocytes.
RTGA zastosovuyut for the diagnosis of a variety of viral illnesses, bugs of such diseases (virus influenza, bark, rubella, tick-borne encephalitis and other) can agglutinate the erythrocytes of various creatures.
mechanism. The typing of the virus is carried out in the hemagglutination galvanization reaction (HTGA) with a set of type-specific serums. The results of the reaction vouch for the day of hemagglutination. Subtype of virus A with antigens H0N1, H1N1, H2N2, H3N2 and in. can be differentiated in RTGA with a set of homologous type-specific serums.
№ 79 Precipitation reaction. Mechanism. components. Methods of staging. Zastosuvannya.
Precipitation reaction (RP)-tse molding and precipitation of a complex of a specific molecular antigen with antibodies in a cloudy appearance, called a precipitate. Vin utvoryuetsya when mixing antigens and antibodies in equivalent quantities; too much of one of them lowers the level of immunity to the immune complex.
RP set in test tubes (reaction of kilceprecipitation), in gels, living media and other.
mechanism. It is carried out with transparent colloidal antigens, extraction of pathological material, objects of the outer environment or pure cultures of bacteria. The reaction of vicorist has clear diagnostic precipitating serotypes with high antibody titers. For the titer of orphans, which precipitates, they take the most diluted antigen, as when interacting with immune orphanage, the elimination of a visible precipitate is turbid.
The reaction of kilceprecipitation put in narrow test tubes (diameter 0.5 cm), add 0.2-0.3 ml of precipitating serum into the pits. Then, with a pasteurized pipette, properly saturate 0.1-0.2 ml of the antigen. Carefully transfer test tubes in a vertical position. The shape of the reaction should be carried out after 1-2 minutes. In times of a positive reaction to the cordon between the grayish and the remaining antigen, a precipitate appears in a seemingly white ring. In the control test tubes, precipitation is not established.
№ 80 Complement binding reaction. Mechanism. components. Zastosuvannya.
Complement fixation reaction (RZK) It is believed that one antigen and one antibody is able to establish an immune complex, until complement (C) is added through the Fc-fragment of the antibody, so that the antigen-antibody complex binds to the complement. If the antigen-antibody complex is not established, then the complement becomes free.
The specific interaction between AG and AT is accompanied by adsorption (binding) to complement. Shards of the process of binding the complement do not manifest themselves visually, J. Bordet and O. Zhang were asked to vicorate as an indicator of the hemolytic system (sheep erythrocytes + hemolytic sirovatka), as it shows that the complement is fixed by the AG-AT complex. Just as AG and AT give one to one, so that the immune complex is established, then the complement is bound by this complex and hemolysis is not observed. If AT becomes AH, then the complex does not settle down and the complement, being depleted of its own, merges with another system and causes hemolysis.
Components Reaction zv'yazuvannya complement (RCC) is brought to folding serological reactions. For this purpose, 5 ingredients are required, and at the same time: AG, AT and complement (the first system), sheep erythrocytes and hemolytic sirovatka (another system).
Antigenome for RZK, there may be cultures of various invaded microorganisms, their licks, components of bacteria, pathological changes and normal organs, tissue lipids, viruses and virus-infected materials.
In the yakost complement vikoristovuyut fresh dry porpoise guinea pig.
mechanism.RCC is carried out in two phases: 1st phase - incubation of the sum, to eliminate the three components of the antigen+antibody+complement; 2nd phase (indicator) - the manifestation of the sum of the free complement by way of adding to it the hemolytic system, which is composed of erythrocytes of the ram, and hemolytic sirovatka, in order to avenge the antibodies to them. In the 1st phase of the reaction, when the antigen-antibody complex is established, binding of the complement to it is observed, while in the 2nd phase, erythrocytes sensitized by antibodies are not detected in hemolysis; the reaction is positive. Although the antigen and antibody do not match one to the other (there is no antigen or antibody in the target group), the complement is left free and in the 2nd phase it comes to the erythrocyte-antithyrocyte antibody complex, inducing hemolysis; reaction is negative. Zastosuvannya.RSK zastosovuyut for the diagnosis of bugs іnfektsiynyh ailments, zokrema syphilis (Wasserman's reaction).
The assistant is made up of seven parts. Part of the first - "Zahalna microbiology" - to avenge the information about the morphology and physiology of bacteria. Part of the friend is dedicated to the genetics of bacteria. The third part - "Microflora of the biosphere" - examines the microflora of the navkolishny middle, its role in the circulation of speech in nature, and also the microflora of the human being and its significance. Part four - "Vchennya about the infection" - is dedicated to the pathogenic power of microorganisms, their role in the infectious process, as well as revenge on antibiotics and their mechanisms. Part of the letter - "Vchennya about Immunity" - to avenge the current notification about Immunity. In the sixth part - "Viruses and ailments, like stinks cry out" - presented in a bridge about the main biological powers of viruses and about those ailments, like stinks cry out. Part of the essay - "Private Medical Microbiology" - to write about the morphology, physiology, pathogenic power of the health workers in various infectious diseases, as well as about modern methods their diagnostics, specific prevention and therapy.
Assistant of appointments for students, graduate students and candidates of higher medical initial mortgages, universities, microbiologists of all specialties and practical doctors.
5th sighting, corrected and added
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Hypersensitivity reactions of the increased type
This type of hypersensitivity is blamed for bugs of infectious diseases, for example, for tuberculosis, brucellosis, dysentery, toxoplasmosis, helminthiasis, mycosis, etc. , to serve as specific diagnostic tests. A hypersensitivity camp of an improved type can induce various medicinal preparations, barniki, antiseptics and other allergens. To allergens of organic and inorganic nature, which may have a low molecular weight, but may still be affected by the proteins of the skin and mucous membranes (those are haptens), often blamed for the so-called contact allergy. Sensitization is formed after trivial contact with such speeches and manifests itself in muscle changes on the skin and mucous membranes. The most typical butt of the increased sensitivity of the improved type is the allergic reaction of the sick people to tuberculosis of people and creatures to tuberculin. Before hypersensitivity reactions of the increased type, transplantation immunity is introduced.
The main features of hypersensitivity of the upgraded type. Hypersensitivity is improved (HCHZ), as the sensitivity of the non-gain type is promoted, it is induced by speeches of antigenic nature and is distinguished by a high immunological specificity, so that it manifests itself only due to the antigen, which is induced її development. At zv'yazku z cim shkirnі alergіchnі tests, yakі viyavlyayut qі become, may have great diagnostic value. The main features of the hypersensitivity of the improved type in relation to the increased sensitivity of the non-gay type of the same.
First, there are those severe reactions that show hypersensitivity of the improved type, a significantly larger term develops after the introduction of the antigen, lower in the case of hypersensitivity of the non-gain type. Zokrema, shkirnі reactions at times vinikayutsya after 6 - 8 years and reach the maximum development after 1 - 2 deb. The intensity of the GCHZ is determined by the diameter of the narrowed cloth of the fabric on the surface of the shkir, with the added hair. In this way, the reaction to the increased sensitivity of the improved type is characterized by the appearance of the effect of negativity.
In another way, the histological picture of the mystic manifestations of hypersensitivity of the upregulated disease is similar to that with the development of sensitivity of the non-gain type of thym, which in the middle of the reaction outweighs lymphocytes and monocytes. In the development of the skin reaction, which shows hypersensitivity of the negaic type, the role of polymorphonuclear leukocytes plays an important role.
Thirdly, the hypersensitivity of the improved type can be passively transferred to a sensitized organism with the help of this serosa to an intact (non-sensitized) organism, i.e., this type of increased sensitivity is associated with antibodies.
The main difference between the reactions of hypersensitivity of the improved type in the reactions of hypersensitivity of the non-gay type in those who stink is mediated not by antibodies, but by sensitized cells - T-lymphocytes, i.e., lymphocytes, yakі have passed immunologists what is the “training” of the thymus. T-lymphocytes carry various specific receptors on their surface, for the help of which they distinguish various foreign speech, including transplantation antigens, and interact with them. All types of hypersensitivity reactions are characterized by a combination of immunological mechanisms, including lymphocytes and humoral factors, which are produced by them. The mediation of these reactions by lymphocytes is confirmed by a variety of phenomena, among which we can see three in front of us.
1. A station of increased sensitivity of the mentioned type can be transferred as a donor to another organism, or by way of introduction to the remaining species of a sensitized organism of yogo lymphocytes, but not antibodies. On the surface of the passive, this type of immune will become, which is transmitted not by the sylvestris, but by lymphocytes, omitting the name of the adoptive (eng. adopt- Nadavati), tobto enraptured. For example, if you pass tuberculin-sensitized creatures internally or intracranial lymphocytes to healthy creatures, then it is not indicative of the introduction of tuberculin by positive skin reactions of hypersensitivity of the increased type .
2. Hypersensitivity reactions of the above type can be suffocated or weakened by introducing an anti-lymphocytic serum before dosing the allergen.
3. With the reaction of GCHZ, it is good to correlate the development of sensitization of T-lymphocytes in synthesizing various mediators - lymphokine, including a factor that inhibits the migration of macrophages (FIM). They are responsible for the stimulation of T-lymphocyte sensitization in vitro by a viable antigen. Addition of a life-giving medium to avenge FIM, to the peritoneal exudates of guinea pigs in glassy vertical capillaries, it is preferable or intermediate between the exudates of leukocytes from capillaries. Unsensitized T-lymphocytes are not subject to authority. Zi zdatnistyu before the reaction coreluє i such a sign of sensitization of T-lymphocytes, as a stimulation of their proliferation in vitro for the help of a viable antigen. T-lymphocytes, which take part in reactions of hypersensitivity of the increased type, signify as T GCHZ, stink may sound like the Lyt-1 + 2 - phenotype, so that specific receptors can be activated, for the help of which they reduce their functions. Populations of such T-HGZ clitins can improve their immunological competence by enriching them with antibodies against antigen receptors. In this way, it can be considered as a residually established that the reaction of HChZ is one of the forms of immune response, which is mediated by sensitization by T-lymphocytes (T HZZ) and appears in the appearance of a characteristic inflammation in the injection site ( sound at shkiri) antigen, which induces її development. In order to show their activity, T HHZ-clitins also require antigens to be presented to them, in addition to MHC molecules of class I or class II. Reactions of HPS (to sensitization of clitin T HPS) can induce various protein antigens - agents that cause contact allergies, and induce antigens of bacteria, viruses, fungi and the simplest. It has been established that cells, similar to clitin T GCHZ, that can detect the Lyt-1 + factor, recognize antitumor antigens and play an important role in anti-tumor immunity.
Moscow State Academy of Veterinary Medicine and Biotechnology named after K. I. Scriabin
Essay
from immunology on the topic:
Allergy. See that mechanism of vindication"
Moscow, 2010 rіk
Allergy.
Allergy (Greek: Allos - іnshhy, ergon - dіya) - reactivity or sensitivity to the body is changed in relation to the third part of speech, often with repeated intake of yoga in the body. The term "alergy" was used in the Austrian teachings of Pirke in 1906 to determine the changed reactivity of the body. Mustard speeches that change the reactive health of the body, arguing to call them allergens. Allergens can be different speeches of a creature's aborosline walk, lipoidi, folding into carbohydrates, lyric speeches and others. Fallow, according to the type of allergens, they distinguish between infectious, kharchov (idiosyncrasy), and medicinal allergies. bud. into the organism. These reactions can be increased in line with the norm - hyperergia, they can be reduced - hypergia - or they can be higher during the day - anergy.
Allergic reactions are subdivided into hypersensitivity of the non-gain type (HNT) and hypersensitivity of the improved type (HRT). HNT is blamed after the repeated introduction of the antigen (alergen) for a sprat of quills, HRT is manifested for a sprat of years (12-48), which is sometimes days. Offensive types of allergies are not less likely to have a clinical manifestation, but the mechanism of their genesis. GNT is associated with antibodies, and the antigen-antibody reaction is at the basis of its genesis. HRT is characterized by the presence of antibodies circulating in the blood, the possibility of passive transmission of hypersensitivity to a normal organism for additional sensitization of T-lymphocytes. Before HNT, anaphylaxis, atopic reactions and syrovatkovu ailment are noted.
Anaphylaxis (Greek: ana - proti, philaxia - zahist) - a camp of increased sensitivity of a sensitized organism to a repeated pararental introduction of a foreign protein. Anaphylaxis first came out of Portia ta Riche in 1902. The first dose of the antigen (protein), which causes increased sensitivity, is called sensitizing (lat. sensabilitas - sensitive), the other dose, after the introduction of which develops anaphylaxis - razdilna zdatnist. Sensitizing dose to administer to creatures sub-shkirno, vnutrishnyom'yazovo, vnutrishnyovenno, vnutrishnyocherevno, razdilnu zdatnist - vnutrishnyovno, vnutrishnyosertsevo, moreover, the razdilna dose is due to buti in a sprat more times. The station of increased sensitivity in creatures develops in 10-20 days. The clinical picture in different species of creatures is not the same. Most defiantly it is seen in guinea pigs. It is necessary to sensitize the guinea pig in advance by introducing 0.01 ml of Kinska sirovatka, and then after 10-20 days to introduce 0.1-0.5 tієї zh of sirovatka, through the sprat of quills a picture of anaphylactic shock develops. The creature starts turbulent, vovna skustuє, the guinea pig smells with paws nіs, there is a sharp ass, a fleeting sight of cuts and feces, tonics and clonic judgments, after 15 whilins the creature is hyne with asphyxia when there is a decrease temperature.
On roztina, emphysema is noted, bleeding is not present, bleeding in the mucous membrane of the mucus membrane, intestines and other organs. Well, as a creature, as if I survived after the shock, I will reintroduce the serum, then there will be no other reaction - the desensitization camp has begun. In humans, that creature anaphylaxis is often blamed for repeated administration of heterogeneous immune siroworts, which are victorious for the prevention of infectious diseases, as well as the administration of certain antibiotics.
IgE and IgG antibodies are vibrated against the primary antigen (protein) in the body. The stench may show signs of cytophilic dominance, either to spores with clitins of a wet type (homocytotropnist) or sporidnenist with clitins of a different species (heterocytotropnist) of creatures. Basically, antibodies are fixed on basophils and dangerous cells. With the repeated introduction of Ag, a specific interaction of the folding complex occurs: the antigen binds with fixation on the cells by antibodies and by the receptors of the cells' surfaces. As a result, the cells are seen as mediators: histamine, serotin, anphylatoxin, bradykinin, heparin, kinin, which correctly reacts with the substance that in, as a clinical picture of anaphylaxis. Also, this form of allergic reaction is associated with the B-lymphocyte system, the proteosynthesis of antibodies is related to the thymus-dependent antigen due to the participation of T-helpers.
