[The most recent advance in clinical investigation of rheumatoid arthritis]

The pathogenesis of rheumatoid arthritis (RA) can be explained through two main hypotheses: T cell-dependent and T cell-independent pathways. The mesenchymal hypothesis has proposed that after an initiation event triggered by T cells, synovitis is maintained by a proinflammatory cytokine cascade, chiefly a TNF-alpha dependent cytokine cascade involving macrophages and synovial fibroblasts. T cells rather may not be important in perpetuating disease at the chronic stages. The T cell hypothesis has proposed that T cells are continuously involved in the pathogenesis of RA from its initiation phase through to the chronic stages. At the latter stages, T cells are importantly concerned in the cytokine network in rheumatoid joints. This paper reviews recent work in this area, and suggests that synergistic approaches targeting the two key aspect of the pathogenesis, T cells and the TNF-dependent cytokine cascade may be the best approach toward attempting a cure of RA.