Rheumatoid arthritis (rheumatoid arthritis) is a chronic, progressive autoimmune disease that mainly affects the joints and leads to systemic inflammation. The pathogenesis of rheumatoid arthritis is multifactorial and is associated with the interaction of genetic predisposition, environmental factors and immune system dysfunction. In the onset of the disease, impaired antigen recognition, activation of T-lymphocytes and β-lymphocytes play an important role. Cytokines, particularly tumor necrosis factor alpha (TNF-α), interleukin-1, and interleukin-6, promote inflammation and synovial tissue destruction in rheumatoid arthritis. Autoantibodies, including rheumatoid factor (RF) and anticyclic citrullinated peptide antibodies (ACPA), are key markers in the diagnosis and prognosis of the disease. Pathologically, rheumatoid arthritis is characterized by hypertrophy of the synovial membrane, pannus formation, and erosion of the joint surface. Studying the immunological mechanisms of rheumatoid arthritis may help develop therapeutic strategies, particularly targeted biologics. These studies are also important in developing therapeutic strategies to prevent chronic inflammation and joint deformity in rheumatoid arthritis.