title: [Cryoglobulinemia and the α-chemokine IP-10].
abstract: IFN-γ-induced protein 10 (IP-10) and its receptor, CXCR3 chemokine (C-X-C motif) receptor 3 (CXCR3), appear to contribute to the pathogenesis of HCV related mixed cryoglobulinemia (HCV+MC). The secretion of IP-10 by CD4+, CD8+ and natural killer (NK)-T cells is dependent on interferon (IFN)-γ, which is itself mediated by the interleukin (IL)-12 cytokine family. Under the influence of IFN-γ, IP-10 is secreted by several cell types including lymphocytes, hepatocytes, endothelial cells, fibroblasts, etc. In tissues, recruited T helper (Th) 1 lymphocytes may be responsible for enhanced IFN-γ and tumor necrosis factor (TNF)-α production, which in turn stimulates IP-10 secretion from the cells, therefore creating an amplification feedback loop, and perpetuating the autoimmune process. High levels circulation of IP-10 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 IP-10 is a novel therapeutic target in HCV+MC.
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: A
authors.initials: A
authors.lastname: Corrado
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: V
authors.initials: V
authors.lastname: Mazzi
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: S M
authors.initials: SM
authors.lastname: Ferrari
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: U
authors.initials: U
authors.lastname: Politti
authors.affiliation: Dipartimento di Scienze Mediche e Chirurgiche Materno-Infantili e dell'Adulto, Università di Modena e Reggio Emilia, Modena, Italia.
authors.forename: D
authors.initials: D
authors.lastname: Giuggioli
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: A
authors.initials: A
authors.lastname: Antonelli
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Università di Pis.
authors.forename: P
authors.initials: P
authors.lastname: Fallahi
authors.affiliation: Dipartimento di Scienze Mediche e Chirurgiche Materno-Infantili e dell'Adulto, Università di Modena e Reggio Emilia, Modena, Italia.
authors.forename: C
authors.initials: C
authors.lastname: Ferri
mesh_terms: D054357:Chemokine CXCL10 / Q000097:blood / Q000378:metabolism*; D003449:Cryoglobulinemia / Q000209:etiology*; D006526:Hepatitis C / Q000150:complications / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D054367:Receptors, CXCR3 / Q000378:metabolism; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology; D013967:Thyroiditis, Autoimmune / Q000209:etiology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C114753:CXCL10 protein, human; C515187:CXCR3 protein, human; D054357:Chemokine CXCL10; D054367:Receptors, CXCR3; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma
keywords: CXCR3, hepatitis C; IP-10; autoimmune thyroiditis; mixed cryoglobulinemia; vasculitis