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Role of CXCL10 in cryoglobulinemia


1, 2, 3, 4, 5, 6

 

  1. Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
  2. Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
  3. Department of Medical, Surgical, Maternal, Paediatric and Adult Sciences, University of Modena and Reggio Emilia, Modena, Italy.
  4. Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
  5. Department of Medical, Surgical, Maternal, Paediatric and Adult Sciences, University of Modena and Reggio Emilia, Modena, Italy.
  6. Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

CER7487
2015 Vol.33, N°3
PI 0433, PF 0436
Review

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PMID: 25571936 [PubMed]

Received: 09/04/2014
Accepted : 18/09/2014
In Press: 08/01/2015
Published: 22/06/2015

Abstract

Interferon (IFN)-γ-induced protein 10 (IP-10/CXCL10) and its receptor, C-X-C motif receptor 3, appear to contribute to the pathogenesis of hepatitis C virus (HCV)-related mixed cryoglobulinaemia (MC) (HCV+MC). The secretion of CXCL10 by cluster of differentiation (CD) CD4+, CD8+, and natural killer-T cells is dependent on IFN-γ, which is itself mediated by the interleukin-12 cytokine family. Under the influence of IFN-γ, CXCL10 is secreted by several cell types including lymphocytes, hepatocytes, endothelial cells, fibroblasts, etc. In tissues, recruited T helper 1 lymphocytes may be responsible for enhanced IFN-γ and tumour necrosis factor-α production, which in turn stimulates CXCL10 secretion from the cells, therefore creating an amplification feedback loop, and perpetuating the autoimmune process. High levels of CXCL10 in circulation have been found in HCV+MC, especially in patients with clinically active vasculitis. Furthermore, HCV+MC patients with autoimmune thyroiditis (AT) have higher levels than those without AT. Further studies are needed to investigate interactions between chemokines and cytokines in the pathogenesis, and to evaluate whether CXCL10 is a novel therapeutic target in HCV-related MC.

Rheumatology Article