Role of interleukin-17 and interleukin 23R gene polymorphism and serum interleukin 17A in rheumatoid arthritis

Document Type : Original Article

Authors

1 assistant lecturer of medical microbiology and immunology faculty of medicine

2 Department of Medical Microbiology and Immunology, Sohag Faculty of Medicine, Sohag University

3 Assistant professor of rheumatology and rehabilitation Sohag University

4 Assistant professor of medical microbiology and immunology Sohag University

Abstract

The multistep process of rheumatoid arthritis (RA), a chronic autoimmune disease, includes the interaction of genetic, environmental, and behavioural risk factors that break immune tolerance and trigger autoimmune processes like the production of autoantibodies, the emergence of the first symptoms prior to the development of clinical arthritis, and finally the appearance of arthritis. In rheumatoid arthritis, the interleukin (IL)-17/IL-23 axis is a crucial pro-inflammatory mechanism (RA). IL-17 is the important factor of inflammation and is contribute to the destruction of bone by increasing the migration of cells, the gene expression of chemokines and the invasiveness of synoviocytes. There are a number of variations in the IL17A gene, and these polymorphisms may affect how IL-17 is expressed. The Th17 has been shown to be more effective than other cells in the development of autoimmune illness. In psoriasis and inflammatory bowel disease patients, IL-23 receptor gene variations were found to raise susceptibilities to autoimmune illness. Investigations also revealed that synovial fibroblasts and plasma from RA patients expressed more IL-23 than normal. Therefore, RA risk may be associated with IL-23 receptor gene variation.

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