New insights in the pathogenesis of rheumatoid arthritis

Abstract

Recent advances in molecular technology as well as clinical research findings have enabled the identification of distinct cell subsets, cell surface markers, and cell products that contribute to the immune mediated inflammation observed in rheumatoid arthritis (RA). However, the lack of definitive insight into the disease etiology has resulted in various hypotheses about the roles of these cells or molecules in the pathophysiology of RA. This review summarizes arguments for and against the central role played by T cells in the initiation and perpetuation of RA. Although the available data do not exclude a role of any particular inflammatory mechanism, understanding of immunoregulatory functions of various T cell subsets may lead to more targeted and effective interventions.