The CXCR3 chemokines in inflammatory myopathies

Clin Ter. 2015;166(1):e56-61. doi: 10.7417/CT.2015.1810.

Abstract

The α-chemokines (C-X-C motif) ligand 9 (CXCL9) and interferon γ-induced protein 10 (IP-10) are expressed in idiopathic inflammatory myopathies muscle. Abundant expression of IP-10 was observed on macrophages and T cells surrounding and invading non-necrotic muscle fibers in polymyositis and sporadic inclusion body myositis and in T cells in perimysial infiltrates of dermatomyositis. IP-10 was also localized to blood vessel endothelial cells in all inflammatory and normal muscle tissues. Serum IP-10 is high in patients with inflammatory myopathies. Human skeletal muscle cells might actively self-promote muscular inflammation by eliciting IP-10 secretion, under the influence of cytokines [Interferon (IFN-γ), Tumor Necrosis Factor (TNF-α)], which can amplify T helper (Th)1 cell tissue infiltration in vivo. It has been shown that drugs able to block the IP-10/chemokine (C-X-C motif) receptor 3 (CXCR3) axis can suppress inflammation in muscle.

Keywords: CCL2; CXCL9; CXCR3; I-TAC; IP-10; Inflammatory Myopathies.

MeSH terms

  • Chemokine CXCL10 / biosynthesis*
  • Chemokine CXCL9 / biosynthesis*
  • Cytokines
  • Humans
  • Inflammation / physiopathology
  • Myositis / physiopathology*
  • Receptors, CXCR3 / biosynthesis*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CXCL10 protein, human
  • CXCR3 protein, human
  • Chemokine CXCL10
  • Chemokine CXCL9
  • Cytokines
  • Receptors, CXCR3
  • Tumor Necrosis Factor-alpha