Dr. S. Louis Bridges and colleagues at UAB have recently shown that the expression of genes encoding receptors for IFNγ are associated with joint damage in rheumatoid arthritis (RA). The study will further explore the role of interferon-gamma (IFNγ) in RA and its severity, as well as the pathogenic mechanisms whereby IFNγ signaling exerts its effects on the clinical manifestations of RA, such as radiographic damage to bones and joints that can lead to significant pain and ultimately disability. By better understanding the pathogenesis of RA through study of signaling pathways, Dr. Bridges and Dr. Raman hope to able to identify additional drug targets to prevent or minimize joint damage and thus avoid disability. Information to be gained from this study can also potentially help to identify new cell signaling targets, perhaps cell-type specific, for RA and autoimmune diseases.
RA and other autoimmune diseases.