Pathophysiology of rheumatoid arthritis.

摘要

PURPOSE OF REVIEW: To provide a summary of recent advances in the pathophysiology of rheumatoid arthritis. RECENT FINDINGS: Highlights include further elucidation of the relationship between the shared epitope, smoking and anticitrullinated protein/peptide antibody generation, including identification of putative citrullinated auto-antigens; and a hypothesis linking citrullinating oral bacteria and anticitrullinated protein/peptide antibody generation. Important work on signalling within regulatory T cells has identified sequestration of protein kinase C theta away from the immune synapse as critical for suppressive activity; TNFalpha exposure interferes with protein kinase C theta compartmentalisation, explaining its inhibition of regulatory T cell function. Platelet microparticles have emerged as important pro-inflammatory mediators via their stimulatory effects on fibroblast-like synoviocytes. The mechanisms by which fibroblast-like synoviocyte invade are becoming elucidated, and recent work suggests the capacity of these cells to migrate from joint to joint, potentially explaining the evolution of clinical rheumatoid arthritis. SUMMARY: Our knowledge of rheumatoid arthritis pathogenesis continues to expand. The last year has seen some key findings, including the identification of novel, potentially tractable targets for further therapeutic research.