Hypersensitivity reactions

In 1975, Jell and Coombs proposed a classification of hypersensitivity reactions, identifying four types. The first three( I-III) of the

are mediated by AT, IV is mediated by T lymphocytes. A number of authors distinguish the V type of hypersensitivity( mixed allergic reactions).

type I - immediate type or anaphylaxis hypersensitivity( lack of protection).In this type of reaction, the Ar-IgE complex binds to the membrane of mast cells or basophils, which leads to the secretion and release of mediators: histamine, chemotactic factors, prostaglandins, thromboxanes, leukotrienes. With the action of mediators on peripheral cells and tissues, a local inflammatory reaction develops, exudation and migration of leukocytes, edema of connective tissue( the result of increased capillary permeability) occurs. The reaction develops within 5-15 min;the outcome depends on the organ in which the allergic reaction occurs( the most dangerous for pulmonary localization).

In clinical practice, local anaphylactic reactions( hay fever, urticaria, food allergy, etc.) are more often observed, however, generalized reactions( anaphylactic shock) are also possible.

II type - cytotoxic immediate reactions - mediated by the AT IgM and IgG, directed against the Arg of the own cells. An immediate damaging effect is the activating complement system or antibody-dependent killer cells( lymphocytes, monocytes).This type of hypersensitivity can be the main one for incompatibility by Rh-factor, autoimmune hemolytic anemia, drug hemolytic anemia, agranulocytosis.

III type - immunocomplex allergic reactions - are mediated by immune complexes, which are aggregates of IgM and IgG with Ar. The formation of such complexes is a natural process that occurs with a normal immune response, but if too many immune complexes are formed, especially unusual sizes, in excess of Ar, their phagocytosis is disturbed, they activate the complement system and cause acute inflammation. The CEC, penetrating the subendothelial space and activating the complement system, causes the development of vasculitis. Later, there is platelet aggregation, leading to blood vessel thrombosis and subsequent tissue necrosis. This type of hypersensitivity is the basis of the reaction of Arthus, allergic alveolitis, skin lesions, joints, kidneys. The peak of the inflammatory reaction is achieved 3-6 hours after exposure to Ar.

IV type - delayed-type hypersensitivity( GGZT) is a cell-mediated( T-lymphocyte) reaction that develops 24-72 hours after the introduction of Ar. Initially trapped in the tissue of Ar is captured by macrophages and is represented by T-lymphocytes. In this case, T-lymphocytes express on their surface a receptor for Ar. An anti-gene-specific clone of T cells is formed. Upon repeated entry of Ar cells, Ar binds through their specific receptors, which causes their proliferation and release of lymphokines. The latter, in turn, locally increase the permeability of the vessels and promote the leukocyte infiltration of tissues at the site of penetration of Ar. Monocytes, macrophages and granulocytes, activated with lymphokines, release the contents of granules( mediators, enzymes) and free radicals in the

tissue, damaging tissues. Reactions of this type occur in infectious and allergic processes, with contact dermatitis and a number of chronic diseases.

V type - mixed allergic reactions - characterized by a combination of different options for immediate and delayed reactions, which are usually observed in most autoimmune and allergic diseases.