CXCL10 and CCL2 Chemokine Serum Levels in Patients With Hepatitis C Associated With Autoimmune Thyroiditis

Antonelli, Alessandro; Ferri, Clodoveo; Fallahi, Poupak; Ferrari, Silvia; Frascerra, Silvia; Pampana, Alessandro; Panicucci, Erica; Carpi, Angelo; Nicolini, Andrea; Ferrannini, Ele

doi:10.1089/jir.2008.0090

Cited by 14 publications

(6 citation statements)

References 35 publications

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“…A paper evaluated CXCL10 levels in patients with CHC in presence/absence of autoimmune thyroiditis (AT) (94). CXCL10 was significantly higher: in AT patients than controls without AT (P<0.001); in patients with CHC than controls without AT, and patients with AT (P<0.001); in patients with CHC and AT than controls without AT, and patients with AT (P<0.001), and hepatitis C (P=0.004).…”

Section: Immune-pathogenesis Of Aitd In Chronic Hcv Infection Cryoglo...mentioning

confidence: 99%

Graves’ disease: Epidemiology, genetic and environmental risk factors and viruses

Antonelli

Ferrari

Ragusa

et al. 2020

Best Practice & Research Clinical Endocrinology & Metab

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163

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Section: Immune-pathogenesis Of Aitd In Chronic Hcv Infection Cryoglo...mentioning

confidence: 99%

Graves’ disease: Epidemiology, genetic and environmental risk factors and viruses

Antonelli

Ferrari

Ragusa

et al. 2020

Best Practice & Research Clinical Endocrinology & Metab

Self Cite

163

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“…Accordingly, the mechanisms of HCV-associated pruritus are attributed to HCV-induced cholestasis and the induction of interferon-stimulated genes (ISGs) as a result of viral overload[ 13 ]. The elevated production of cytokines ( e.g ., IL-8) and chemokines ( e.g ., CCL2, CXCL1 and CXCL5) during the course of cholestatic hepatitis C[ 14 - 17 ], is expected to be the main mediators for the induction of HCV-associated pruritus.…”

Section: Mechanisms Of Hcv Infection and Treatment- Associated Pruritmentioning

confidence: 99%

Hepatitis C virus-associated pruritus: Etiopathogenesis and therapeutic strategies

Alhmada¹,

Selimović²,

Murad³

et al. 2017

WJG

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In addition to its contributing role in the development of chronic liver diseases, chronic hepatitis C virus (HCV) infection is associated with extrahepatic manifestations, particularly, cutaneous-based disorders including those with pruritus as a symptom. Pruritus is frequently associated with the development of chronic liver diseases such as cholestasis and chronic viral infection, and the accumulation of bile acids in patients’ sera and tissues as a consequence of liver damage is considered the main cause of pruritus. In addition to their role in dietary lipid absorption, bile acids can trigger the activation of specific receptors, such as the G protein-coupled bile acid receptor (GPBA/ TGR5). These types of receptors are known to play a crucial role in the modulation of the systemic actions of bile acids. TGR5 expression in primary sensory neurons triggers the activation of the transient receptor potential vanilloid 1 (TRPV1) leading to the induction of pruritus by an unknown mechanism. Although the pathologic phenomenon of pruritus is common, there is no uniformly effective therapy available. Understanding the mechanisms regulating the occurrence of pruritus together with the conduction of large-scale clinical and evidence-based studies, may help to create a standard treatment protocol. This review focuses on the etiopathogenesis and treatment strategies of pruritus associated with chronic HCV infection.

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“…Interestingly, the fact that in MC patients circulating CXCL10 is significantly higher in the presence of AT, compared to patients without thyroiditis, while CCL2 (the prototype Th2 chemokine) is comparable, suggests that the Th1 CXCL10 chemokine is specifically linked with the appearance of AT in these patients [66,69].…”

Section: Thyroid Disorders Associated With Chcmentioning

confidence: 99%

Cytokines and HCV-related autoimmune disorders

et al. 2014

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Cytokines are intercellular mediators involved in viral control and liver damage being induced by infection with hepatitis C virus (HCV). The complex cytokine network operating during initial infection allows a coordinated, effective development of both innate and adaptive immune responses. However, HCV interferes with cytokines at various levels and escapes immune response by inducing a T-helper (Th)2/T cytotoxic 2 cytokine profile. Inability to control infection leads to the recruitment of inflammatory infiltrates into the liver parenchyma by interferon (IFN)-γ-inducible CXC chemokine ligand (CXCL)9, -10, and -11 chemokines, which results in sustained liver damage and eventually in liver cirrhosis. The most important systemic HCV-related extrahepatic diseases-mixed cryoglobulinemia, lymphoproliferative disorders, thyroid autoimmune disorders, and type 2 diabetes-are associated with a complex dysregulation of the cytokine/chemokine network, involving proinflammatory and Th1 chemokines. The therapeutical administration of cytokines such as IFN-α may result in viral clearance during persistent infection and revert this process. Theoretically agents that selectively neutralize CXCL10 could increase patient responsiveness to traditional IFN-based HCV therapy. Several studies have reported IL-28B polymorphisms and circulating CXCL10 may be a prognostic markers for HCV treatment efficacy in HCV genotype 1 infection.

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CXCL10 and CCL2 Chemokine Serum Levels in Patients With Hepatitis C Associated With Autoimmune Thyroiditis

Cited by 14 publications

References 35 publications

Graves’ disease: Epidemiology, genetic and environmental risk factors and viruses

Graves’ disease: Epidemiology, genetic and environmental risk factors and viruses

Hepatitis C virus-associated pruritus: Etiopathogenesis and therapeutic strategies

Cytokines and HCV-related autoimmune disorders

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