Abstract
Background. Rheumatoid arthritis (RA) is a multietiological chronic systemic autoimmune disease associated with inflammatory joint damage and extra-articular processes in internal organs. RA is recognized as the most common autoimmune inflammatory arthritis with an incidence of 0.4% to 1.3% of the population. Objective. Summarize current information on the immunopathogenesis of RA based on data from open sources of information. Methods. The selection of publications that covered information about the immunopathogenesis of rheumatoid arthritis was performed using the following keywords: systemic autoimmune diseases, RA, citrullination, carbamylation. Results. RA is considered an immune-mediated disease with a strong genetic influence. An important role in the initiation of the development of RA is played by genetic factors and damage to the mucous membranes in the lungs, oral cavity, and gastrointestinal tract.. In response to the appearance of post-translationally modified (citrullinated/carbamylated) proteins, B-cells induce the production of antibodies to cyclic citrullinated peptide (anti-citrullinated peptide antibodies – ACPA). Rheumatoid factor is another well-studied autoantibody involved in the development of RA. Given the complex role that dendritic cells play in the pathogenesis of RA, targeted therapies are being developed to block their immunogenic or enhance their tolerogenic functions. Dysfunction of fibroblast-like synoviocytes leads to synovial hyperplasia. Disease-modifying antirheumatic drugs (DMARDs) are used to target inflammation and prevent disease progression. Conclusions. Genetic predisposition and specific post-translational modifications of proteins play a significant role in the development of RA. The introduction of DMARDs and the prospects for the use of mesenchymal stem cells and their derivatives allows for the development of new effective treatment strategies to implement more effective control over this disease.
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