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Endogenous and exogenous factors as triggers of process of an autoimmune inflammation

Pseudorheumatism as the typical representative of autoimmune inflammatory diseases is the multifactorial disease which exact reason is unknown. These factors, in turn, can be parted on exogenous and endogenous.

Genetic predisposition, first of all, concerns internal causes, to exogenous - infectious agents, toxic substances, environment factors.

In favour of genetic predisposition says that fact that there is a hereditary predilection to development of autoimmune diseases. It has been counted up, that risk of development juvenilnogo a pseudorheumatism at siblingov in 15 times above, than in population [137].

The basic genetic marker identified with a pseudorheumatism, is HLA (a human leukocytic antigen). It is established, that carriers HLA-DR1/HLA-DR4 have larger risk of development rhematoid
Arthritis [52]. Besides it, carriage HLA-B27 assotsiirovano with an ankylosing spondylitis [21,77].

PTPN22 (protein tyrosine phosphatase non-receptor 22) the gene codes limfoidnoyospetsificheskuju fosfatazu (Lyp). The variant in coding area of this gene which as it is informed, is bound to a number of autoimmune diseases, also has been defined as a susceptibility locus to JURA. Effects PTPN22 differ between forms JURA, but, in general a little, are more consecutive, than genes HLA [18].

Some other genes, including the factor ingibitsii macrophages, ИЛ-6, ИЛ-10 and the factor of a necrosis of a tumour FNO, also are bound with JURA in various populations and at different forms [199]. Also some other polymorphisms, such as GSTnull, CTLA4, CD244, PADI4, SLC22A2 can raise risk of development of a pseudorheumatism [15,74,208]. Nevertheless, these genes can collectively make only small share from the general genetic contribution to illness. Influence of various polymorphisms on efficiency of spent therapy of a pseudorheumatism [75] is besides, described.

Infectious diseases concern the basic exogenous trigger factors, first of all. In researches it was revealed, that at 20 % of patients with an early pseudorheumatism the infection acted in a role of the initiating factor [144]. In particular, antibodies to Epstein-Barr virus are taped in a high caption at 80 % of patients with a pseudorheumatism. Higher frequency of a becoming infected of lymphocytes of patients RA in comparison with cells of healthy donors is taped. In experiment development of an arthritis in mice caused culture of the retroviruses allocated from sinovialnoj of a liquid of patients RA. There is a point of view that the virus infection can start process of polyclonal V-cellular activation with the subsequent synthesis of rhematoid factors by plasmocytes, as is observed at a pseudorheumatism [1]. Besides, hypothetical triggers of rheumatic diseases are: viruses of the simple herpes surrounding
Depriving, a cytomegalovirus, T-limfotropnyj a virus, viruses of a parotitis, a measles, respiratorno-sintsitialnoj a virus, a hepatitis virus In [20,81,206].

Besides, there are the data specifying in possibility of participation in quality of triggers of toxic substances, such as mercury; deficiency nutrientov, first of all vitamins and minerals, and other irreplaceable nutrients; a food allergy [155].

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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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