Modern representations about a pathogenesis of rheumatic diseases

The character of the immune answer in many respects defining features of development immunopatologicheskih of processes at diseases of the person, depends on primary activation of two subpopulations CD4 + T-limfotsitov - Th1 and Th2 cells which synthesise cytokines with various immune effects.

To the cytokines synthesised Th1 by cells, carry ИЛ-2, ИЛ-12, interferon (ИФН-y) and the factor of a necrosis tumours (TNF)-u/r, and to Th2 to cytokines - ИЛ-4, ИЛ-5, ИЛ-6, ИЛ-13 and ИЛ-10. It is supposed, that Th2 cytokines provide first of all reactions of humoral immunity (synthesis of antibodies and autoantibodies) while Th1 cytokines are involved in reactions of cellular immunity (hypersensitivity of the slowed down type, cellular cytotoxicity and an inflammation). Prominent feature of corresponding cytokines is ingibitsija differentiations and effektornyh functions retsiproknyh phenotypes Th of cells. For example, ИФН-yи ИЛ-12, stimulate Th1 cells and suppress proliferation Th2 of cells, and ИЛ-4 and ИЛ-10 opposite stimulate Th2 and inhibit Th1 cells. It is necessary to underline, that for HARD CURRENCY and other inflammatory rheumatic diseases such defects immunoreguljatsii which lead to abnormal production of cytokines of both types are characteristic. Moreover their synthesis can essentially vary in various phases
Diseases. Nevertheless taking into account a prevailing profile of synthesis of cytokines conditionally allocate so-called "Th1 - and Th2-dependent diseases". At HARD CURRENCY the generalised V-cellular hyperreactivity combined with weakening of cellular immunologic reactions which associates with depression of synthesis Th1 of cytokines (ИЛ-2, ИФН-yи ИЛ-12) and hyperproduction ИЛ-10 (Th2 a cytokine) is observed. Therefore the HARD CURRENCY is surveyed as a prototype of Th2-dependent diseases [3]. At a pseudorheumatism autoimmune activation T-limfotsitov on Th1 to the type, characterised by superfluous synthesis ИЛ-2, ИФН-yи ИЛ-17, and leading disbalansu between a hyperproduction of proinflammatory cytokines mainly makrofagalnoj the nature, such as the factor of a necrosis FNO, ИЛ-1, ИЛ-6, ИЛ-8 and antiinflammatory cytokines (ИЛ-4, ИЛ-10, soluble antagonist ИЛ-1, soluble ФНО-a receptors), with prevalence of production of the first over the second is observed. Thus, the pseudorheumatism is surveyed as a prototype of Th1-dependent diseases [2].

Recently many researchers take away the leading part in a pathogenesis of the rheumatic diseases T-limfotsitam, producing ИЛ-17 (Th17). Th17 cosecrete ИЛ-17, ИЛ-22, ИЛ-6 and FNO. ИЛ-17 - plejotropnyj a cytokine, which acts as a mediator of a fabric inflammation by an induction of set of proinflammatory cytokines (such as ИЛ-6, FNO) [122,141]. Recently Th17 the role primary effektornyh cells in development of autoimmune diseases, both in the person, and in mice [104,113,211,216] is attributed. Raised expression ИЛ-17 has been found out in blood serum and target tissues of patients with such diseases, as a pseudorheumatism, a multiple sclerosis, a system lupus erythematosus [57,123].

Besides it, there are data confirming participation plazmatsitoidnyh dendritic cells (also known as IFN-AV-PRODUCING cells) in development of some autoimmune diseases, such as a pseudorheumatism, HARD CURRENCY, a psoriasis arthritis, a multiple sclerosis, syndrome SHegrena [10,102].


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Scientific source EGOROV Andrey Sergeevich. THE GEPSIDIN-INTERLEUKIN-6 SYSTEM AS A FACTOR FOR MANAGING THE COURSE OF ANEMIA IN CHRONIC ARTHRITIS IN CHILDREN DISSERTATION for the degree of candidate of medical sciences. St. Petersburg - 2016. 2016

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