Abstract
Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. Some of these antibodies are present in the patients' serum several years before the onset of clinical disease. Various genetic and environmental factors are associated with autoantibody production against different autoantigenic targets. Both the activating and inhibitory FcγRs and the activation of different complement cascades contribute to the downstream effector functions in the antibody-mediated disease pathology. Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed for early diagnosis of the clinical disease. Recently, a direct link was proposed between the presence of autoantibodies and bone erosion as well as in the induction of pain. In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and the significance of IgG-Fc glycosylation are discussed.
Highlights
Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, which affects approximately 1% of the world population, and is characterized by autoantibody production, synovial inflammation, cartilage destruction, and bone erosion [1]
A large number of studies have found that abnormally increased immune cells (T cells, B cells, macrophages, and neutrophils) and immune molecules are present in the synovial tissue and fluid of RA patients, which suggest that the release or activation of them may be involved in the initiation and perpetuation of RA
rheumatoid factors (RF) has been widely used in the diagnosis of RA since its discovery in 1940 as an antibody directed against serum gamma-globulin, which promoted the agglutination of sheep red blood cells sensitized by subagglutinating doses of rabbit antibodies [41]
Summary
Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, which affects approximately 1% of the world population, and is characterized by autoantibody production, synovial inflammation, cartilage destruction, and bone erosion [1]. In RA, an increased number of autoantibodies directed against these self-antigens such as rheumatoid factors (RF) and anticitrullinated protein antibody (ACPA) are commonly prevalent. The discovery of new specific autoantibodies to improve the early diagnosis rate has become a hot topic in current research. More than ten autoantibodies related to RA were identified, which have greatly helped to develop new early diagnosis and prognosis methods. How specific autoantibody responses change and evolve over time to become more pathogenic, interactions between different autoantibody types, their synthesis, and the role of Fc glycosylation will be discussed. The implications of these findings for the clinical practice are briefly discussed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
