TNF and IL-1 in particular play a significant role in the inflammatory process of joints in RA. In addition, the overproduction of inflammatory molecules, tumour necrosis factor (TNF), prostaglandin E2 (PGE2), interleukin (IL)-1 and cytokines induces chronic inflammation. The B cells, macrophages and CD4+ helper T cells infiltrating the synovial stroma result in the spread of the synovium, which causes swelling and pain in the joints. What is characteristic of RA is the appearance of pathological changes, which first occur in the joint lining. Attention is drawn to the antigenic similarity of some bacteria or viruses and HLA-DRB1 and HLA-DRB4 histocompatibility antigens, often present in RA patients, which is conducive to the initiation of the autoimmune process. Additionally, a previous infection, especially viral, translates into the stimulation of the immune system in response to infection, which, in people predisposed to RA, may trigger an autoimmune reaction directed against the joint structures. In such cases, the disease is characterised by a more severe clinical course. The consequence of polyclonal B cell activation and excessive humoral immune response is the production of various autoantibodies, including RF, the presence of which is found in approximately 80% of RA patients. Some of them are disorders of the acquired immune response-they participate in the initiation and maintenance of disease development, with a special role of T lymphocytes recognising the body’s own antigens, e.g., citrullinated autoantigens, and supporting the production of autoantibodies with the same specificity, e.g., anti-CCP antibodies.
Several factors can influence the development of the disease. Up to 60% of the risk for developing RA can be attributed to environmental susceptibility factors, but not many of them have been identified to date.
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