Rheumatoid arthritis is an auto-immune disorder, recognized by cartilage as well as bone destruction, which causes irreversible joint deformities, which further results in functional limitations in the patient. Genes like HLA-DRB1 and PTPN22 are likely implicated in the genetic predisposition of rheumatoid arthritis pathology. The first and foremost clinical manifestation in a person with rheumatoid arthritis is joint destruction followed by cartilage and bone destruction caused by cell-cell interactions. The cell-cell interactions are thought to be initialized through the contact of antigen-presenting cells (APC) with CD4+ cells, leading to the progression of the disease. APC includes a complex of class ІІ major histocompatibility complex molecules along with peptide antigens and binds to the receptors present on the surface of T-cells. Further, the activation of macrophages is followed by the release of various pro-inflammatory cytokines such as IL-1 and TNF-α, which lead to the secretion of enzymes that degrade proteoglycan and collagen, which in turn, increase tissue degradation. Biomarkers like IL-6, IL-12, IL-8 and IL-18, 14-3-3η, RANKL, IFN-γ, IFN-β and TGF-β have been designated as key biomarkers in disease development and progression. The study of these biomarkers is very important as they act as a molecular indicator of pathological processes that aggravate the disease.
Keywords: Arthritis; C4D+.; antigen-presenting cells; biomarkers; inflammation; joint destruction.
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