Rheumatoid Arthritis and the Th1 Chemokine MIG

Clin Ter. Nov-Dec 2019;170(6):e472-e477. doi: 10.7417/CT.2019.2178.

Abstract

Monokine induced by interferon (IFN)-γ (MIG) and its receptor chemokine (C-X-C motif) receptor 3 (CXCR)3 seem to play an important role in the pathogenesis of rheumatoid arthritis (RA). MIG expression has been observed in sera, synovial fluid (SF) and synovial tissue of RA patients; it is highly expressed in RA synovium by infiltrating macrophage-like cells and fibroblast-like synoviocytes. A Type-1 helper-response orientated disease was suggested because of the high expression of CXCR3 in SF T cells and the presence of elevated IFN-γ levels. It has been observed a decrease of the inflammation by anti-CXCR3, and anti-MIG molecules, in fact they inhibit CXCR3-enhanced cell migration and pro-inflammatory cytokine expression, leading to an amelioration of the arthritis progression. These findings suggest a possible therapeutic role of these molecules in humans.

Keywords: MIG; Rheumatoid arthritis.

Publication types

  • Review

MeSH terms

  • Arthritis, Rheumatoid / metabolism*
  • Chemokine CXCL9 / metabolism*
  • Humans
  • Receptors, CXCR3 / metabolism
  • Synovial Fluid / metabolism
  • T-Lymphocytes / metabolism

Substances

  • CXCL9 protein, human
  • CXCR3 protein, human
  • Chemokine CXCL9
  • Receptors, CXCR3