Research Summary

Understanding the influence of inflammatory cells on bone cells in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is one of the most common autoimmune disorders with an estimated global prevalence of 0.3 to 1 percent and is 2-3 times more frequently observed in women than men. The disease is characterized by chronic synovial inflammation leading to the progressive joints destruction and disability. Inflammation is central to the pathogenesis of RA and inflammatory cytokines are therefore attractive therapeutic targets for RA. Over the past two decades, several cytokines have been implicated in the pathogenesis of RA and tested for their therapeutic potential. Biologics targeting the key inflammatory cytokines are already approved for therapeutic use in RA but are associated with several side effects that make their persistent administration concerning. Moreover, in RA sustained treatment-free remission is rarely observed with biologics.

Therefore, understanding RA pathogenesis is extremely essential for the search of newer inflammatory molecules for eventual delineation of therapeutic targets. My current research in RA is focused towards understanding following aspects: 1) how cytokines are positioned in the complex cytokine network in synovial inflammation? 2) How to boost self tolerance. 3) How immune cells and their mediators influence bone homeostasis? 4) Cross talk between immune and  bone cells.