Exploring the influences on rheumatoid arthritis progression: A comprehensive review of autoimmunity and cellular mechanisms

Abstract

This review revealed the complex relationship between autoimmunity and Rheumatoid Arthritis (RA), emphasizing the importance of understanding various intrinsic and extrinsic factors contributing to disease progression. RA, affecting 1 % of the world's population, predominantly impacts females and presents clinical symptoms such as joint swelling and morning stiffness. Biomarkers like RF and ACPA are used for disease prognosis. Autoimmunity, characterized by the immune system's attack on self-cells, leads to the production of autoantibodies against self-biomolecules, initiating cellular impairment and disease onset. Our review aims to comprehensively synthesize the myriad risk factors involved in RA progression, encompassing genetic, epigenetic, cellular, and environmental determinants. These factors contribute to the production of autoantibodies and shape the autoimmune milieu within RA. The autoimmune nature of RA, demonstrated by the presence of ACPA and other autoantibodies, triggers immune responses and proinflammatory cytokine release, stimulating synovial fibroblast activity and joint destruction. Furthermore, aggressive epigenetically modified synovial fibroblasts play a role in disease pathology. In this article, we highlighted the significance of understanding immune tolerance alterations related to autoimmune diseases like RA and advocated for studying similar factors in other diseases to enhance our understanding of RA pathophysiology. Advances in clinical investigations, such as using RA-specific peptides or proteins and cell-based therapies, showed promise in improving RA patient outcomes. Overall, our review aims to provide valuable insights into the intricate mechanisms driving RA progression, offering potential avenues for therapeutic intervention and disease management.