Rheumatoid arthritis and the Th1 chemokine MIG

doi: 10.7417/CT.2019.2178

  • S.R. Paparo Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy

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

Published
2019-11-06
How to Cite
PAPARO, S.R.. Rheumatoid arthritis and the Th1 chemokine MIG. La Clinica Terapeutica, [S.l.], v. 170, n. 6, p. e472 - e477, nov. 2019. ISSN 1972-6007. Available at: <http://www.clinicaterapeutica.it/ojs/index.php/ClinicaTerapeutica/article/view/529>. Date accessed: 15 nov. 2019.