The TIM-3/Gal-9 Pathway: A Promising Therapeutic Target for Regulation of Immune Checkpoint in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune ailment that is marked by persistent synovial joint inflammation, which causes joint destruction and other systemic consequences. The immune system is equipped with a wide range of effector mechanisms that are capable of inflicting severe harm on pathogens that invade it, as well as inflicting severe harm on the body itself. The immune system must carefully regulate itself to avoid such damage to host tissues and restore equilibrium following an inflammatory response. In the peripheral immune system, the immune cell responses are regulated by a balance of positive and negative signals that are sent to effector cells to adjust them to their environment. The identification of immunological checkpoints has opened up new avenues for studying and perhaps modifying immune responses in the context of RA pathogenesis. T-cell immunoglobulin and mucin domain-containing molecule 3 (TIM-3), a member of the TIM family, has emerged as a major regulator in immune checkpoint pathways, with several studies on its various functions in immunological homeostasis and autoimmune disorders. This review narrates the critical function of TIM-3 in the control of immunological checkpoints in rheumatoid arthritis also the potential role of TIM-3/GAL-9 signalling as a therapeutic target for the development of a new class of immunotherapeutic agents for the treatment of RA.