Keywords
etiology
pathogenesis
synovial tissue
immunocompetent cells
T-lymphocytes
B-lymphocytes
macrophages
cytokines
How to Cite
Abstract
This review reflects modern ideas about the etiology and pathogenesis of Rheumatoid arthritis (RA). The disease is believed to be caused by various external or internal stress factors in individuals with a genetic predisposition. Under modern concepts, RA is an autoimmune disease, and the basis of its pathogenesis is the defects of the regulatory mechanisms providing the activation of the immune system against various stimuli. The onset of RA is in the peripheral lymphoid organs. Dendritic cells activate T-lymphocytes, activating B-lymphocytes through cytokines and costimulatory molecules, and cause the synthesis of autoantibodies, the accumulation of immune complexes in the joints, and the development of rheumatoid synovitis. B-lymphocytes secrete rheumatoid factor (RF), antibodies to cyclic citrulline peptide (ACCP), and proinflammatory cytokines and also activate T-lymphocytes by indicating signaling molecules. During T-lymphocyte activation, CD4+ Th-cells interact with HLA, MHC-II molecules, and costimulatory molecules located on the surface of antigen-presenting cells. This interaction activates a signaling pathway leading to the maturation of CD4+ cells, resulting in the activation of pro-inflammatory CD8+ T-lymphocytes. CD4+ Th cells also play an important role in RA regeneration through the secretion of cytokines and chemokines, the important immunomodulators of cellular immunity.
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