84. III hypersensitivity reaction , mechanism and scheme of the reaction, examples of diseases.

Type III hypersensitivity – Immunocomplex reactions

In immunocolplex lesions, antibodies attach to antigens and then cause inflammation directly or by activating complement. Leukocytes (neutrophils and monocytes) produce tissue damage by lysosomal enzymes and the generation of toxic free radicals.

Reaction rate – hours-days

It is mediated by IgG, IgM, IgA as part of immune complexes

Chemical mediators of damage - complement and its fractions

Mechanism - accumulation of neutrophils, macrophages; release of lysosomal enzymes

(more details on the mechanism below):

The complexes linger in tissues (often unrelated to the source of hypertension) and trigger local or systemic inflammatory reactions. By binding and activating complement components, they attract phagocytic cells (macrophages, neutrophils). The latter are unable to absorb such large structures and secrete proteolytic enzymes and other inflammatory mediators that damage the tissues in which the complex is fixed. A typical manifestation of reactions of the third type is the Arthus phenomenon.

Clinical examples of type III reactions are serum sickness (after ingestion of foreign proteins or medications into the bloodstream), exogenous allergic alveolitis (after fixation of complexes in pulmonary capillaries), systemic lupus erythematosus, rheumatoid arthritis (after fixation of complexes in the synovial membranes of joints), vasculitis (with lesions of the endothelium of blood vessels), glomerulonephritis (during fixation complexes in the filtering apparatus of the kidneys).

85. IV hypersensitivity reaction , mechanism and scheme of the reaction, examples of diseases.

Mediate the reactions of T cells - TH1 (CD4+) and TH2 (CD8+), sensitized by local contact with antigen (antigen-specific T cells); antibodies are not involved in the implementation of reactions of this type

TD memory cells are involved:

• The first contact causes sensitization

• Subsequent contacts - implementation of the reaction

Reactions are delayed for one or more days or weeks (delayed type of hypersensitivity) – The delay is explained by the migration of macrophages and T cells to the site of exposure to foreign antigens

Activation of cytokines or cytotoxins causes damage, or macrophages and NK cells are activated

Activated T cells can act in two ways:

• CD4+ T cells secrete cytokines that activate macrophages that phagocytize cells (delayed type of hypersensitivity)

• CD8+ T cells directly "kill" target cells (direct cellular cytotoxicity

Clinical and morphological manifestations of HRT: tuberculin-type reaction on the skin in response to antigen administration, contact dermatitis (contact allergy), autoimmune diseases, reactions in many viral and some bacterial (viral hepatitis, tuberculosis, brucellosis) infections. Granulomatosis is also a morphological manifestation of HRT.

An example of a HRT reaction: I am the body's response to intradermally injected tuberculin, a component from the walls of Mycobacterium tuberculosis. In a sensitized patient, redness and compaction occur at the injection site after 8-12 hours, and the peak of the reaction occurs after 24-72 hours. Necrosis develops in significantly sensitized patients in the injection area. HRT is characterized by the accumulation of mononuclear cells in subcutaneous tissue and dermis, mainly around small veins and venules with the formation of characteristic perivascular cuffs. The release of plasma proteins beyond the vascular bed increases edema of the dermis and is accompanied by the deposition of fibrin in the interstitium. With the persistence of the antigen, macrophages transform into epithelioid cells surrounded by a shaft of lymphocytes - a granuloma is formed