Biomarker Approach Towards Rheumatoid Arthritis Treatment

Curr Rheumatol Rev. 2021;17(2):162-175. doi: 10.2174/1573397116666201216164013.


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.

Publication types

  • Review

MeSH terms

  • Arthritis, Rheumatoid / etiology
  • Arthritis, Rheumatoid / metabolism*
  • Arthritis, Rheumatoid / therapy
  • Biomarkers / metabolism
  • Cytokines / metabolism*
  • Humans
  • Molecular Targeted Therapy


  • Biomarkers
  • Cytokines