Rheumatoid Arthritis: What Inflammation Do We Face?

• Published in: Journal of Molecular Pathology 2024-10, Vol.5 (4), p.454-465
• Main Authors: Poznyak, Anastasia V., Kirichenko, Tatyana Vladimirovna, Beloyartsev, Dmitry Felixovich, Churov, Alexey V., Kovyanova, Tatiana Ivanovna, Starodubtseva, Irina Alexandrovna, Sukhorukov, Vasily N., Antonov, Stanislav A., Orekhov, Alexander N.
• Format: Article
• Language: English
• Subjects: Adaptive immunity; autoimmune disease; Autoimmune diseases; Bacterial infections; BLyS protein; Bone resorption; Cartilage; CD14 antigen; CD16 antigen; CD4 antigen; Cell activation; Cell proliferation; Chemokines; CXCL10 protein; CXCL12 protein; Cytokines; Disease; Enzymes; Fibroblasts; immune response; Immune system; Immunological tolerance; Immunoregulation; Infections; Inflammation; Innate immunity; Interleukins; Lymphocytes T; Macrophages; Microbiomes; Monocyte chemoattractant protein 1; Monocytes; Neutrophils; Pathogenesis; Pathogens; Peptides; Proteins; Rheumatoid arthritis; Trauma; Tumor necrosis factor-α
• ISSN: 2673-5261; 2673-5261
• DOI: 10.3390/jmp5040030

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by symmetrical joint inflammation, cartilage degradation, and bone erosion. This review explores the multifaceted aspects of RA pathogenesis, focusing on the dynamic interplay between innate and adaptive immune responses, genetic predisposition, and environmental triggers. The development of RA involves genetic susceptibility and trigger events such as infections, trauma, smoking, obesity, and microbiome alterations, fostering autoimmune reactions and tissue/organ destruction. The innate immune response, including toll-like receptor activation and synovial fibroblasts’ roles, contributes to the acceleration of inflammatory processes in joint tissues. Monocytes and macrophages organize and sustain chronic joint inflammation, leading to tissue damage and bone resorption, while highlighting the significance of CD14 and CD16 subsets in RA pathogenesis. In the adaptive immune response, aberrant activation and proliferation of CD4+ T cells and the role of regulatory T cells in maintaining immune tolerance are discussed. Target cytokines like TNF-α, IL-6, IL-1, IL-17, and BAFF, as well as chemokines such as CCL2, CXCL10, CCL5, and CXCL12, have emerged as critical components in managing chronic inflammation and joint damage in RA. This comprehensive overview provides insights into the pathophysiology of RA and potential therapeutic avenues, emphasizing the importance of understanding these complex immunological and genetic mechanisms for developing more effective treatment strategies.