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.