Role of T cells and cytokines in the pathogenesis of rheumatoid arthritis

Rheumatoid arthritis (RA) is a long-term autoimmune disease. It causes persistent joint inflammation, aberrant tissue growth, and progressive joint deterioration. T cells have a key role in the onset of RA. They identify and trigger other immune cells, and produce inflammatory signals such as interleukin-6 (IL-6), interleukin-17 (IL-17), and tumor necrosis factor-α (TNF-α). Prolonged inflammation and tissue damage are caused by an imbalance between regulatory T cells (Tregs) and pro-inflammatory T helper 17 (Th17) cells. Additionally, the condition is exacerbated by uncontrolled cytokine networks and autoantibody formation. This study highlights the significance of biomarkers, cytokine signaling, and the imbalance of T cell subsets in RA for treatment. Along with updates from clinical trials, we also discuss T cell-focused therapeutics, PD-1/PD-L1 regulation, and Treg adoptive therapy. Finally, we address significant issues and RA's future prospects. • Autoantigens activate CD4 + T cells, releasing IL-17 and TNF-alpha, causing joint inflammation. • Cytokines attract immune cells, promoting pannus formation and bone damage. • Dysregulated Th1, Th2, Th9, and Th17 subsets lead to chronic inflammation. • Dysfunctional Tregs fail to control immune responses, cause autoimmunity in RA. • Activated T cells stimulate B cells to produce auto antibodies.