Immunopathology of Rheumatoid Arthritis
Date
2024-08-06
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Abstract
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The immunopathology of rheumatoid arthritis (RA) is very complex and not fully understood as there are a variety of factors that work together to result in the development of this disease. Genetic predispositions such as certain HLA haplotypes as well as environmental factors such as cigarette smoking, infections, and other factors may lead to the initial break in self-tolerance before the development of clinical RA. During this preclinical or asymptomatic phase, there may be manifestations of systemic autoimmunity such as the presence of autoantibodies and inflammatory cytokines. Many studies have demonstrated that antibodies such as anti-citrullinated protein antibodies (ACPA), rheumatoid factor (RF), and anti-carbamylated protein (CarP) antibodies can be present for years before the development of RA (Brink et al.). However, the presence of these antibodies may be reversible and self-limiting (Hans Ulrich Scherer et al.). When cells experience repetitive triggering, this transient systemic autoimmunity can become persistent which ultimately leads to the development of clinical disease (Hans Ulrich Scherer et al.). During this early process, as the autoantibody B cell response evolves after the initial break in self-tolerance, HLAs play a major role in the pathogenesis of RA, thus highlighting the involvement of T cells in the development of clinical disease (Hans Ulrich Scherer et al.).
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Keywords
rheumatoid arthritis, pathology, immunology, shared epitope, rheumatoid factor, HLA, anti-citrullinated protein antibodies (ACPA)