The signal transducer and activator of transcription factors lodge in immunopathogenesis of rheumatoid arthritis

Rheumatoid arthritisis (RA) is a chronic autoimmune disorder that affects ~1-2% of the world’s population and damages synovial joints. RA is characterized by inflammation, autoantibody production, cartilage and bone destruction and synovial hyperplasia. Inflammation induces systemic and articular synthesis of pro-inflammatory cytokines, such as tumor necrosis factor alpha and interleukin-6 that play essential roles in joint and other organ damage in this disease. Considering the role of signal transducer and activator of transcription factors (STATs) in signaling of these cytokines, these proteins may be involved in the pathogenesis of RA. The expression and activity of STATs can contribute to the onset, progression and severity of RA. All STAT family members (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, and STAT6) have been associated with autoimmune diseases, as highlighted in several studies. In this review we aim to describe the immunobiology of STATs and its family members and the role of these proteins in the immunopathogenesis of RA.