Role of chemokines and their receptors in viral persistence and liver damage during chronic hepatitis C virus infection
Authors
Larrubia , Juqan Ramon; Benito Martínez, Selma; Calvino Fernández, Miryam; Sanz De Villalobos , Eduardo; Parra Cid, TrinidadIdentifiers
Permanent link (URI): http://hdl.handle.net/10017/59281DOI: 10.3748/wjg.14.7149
ISSN: 1007-9327
Date
2008Affiliation
Universidad de Alcalá. Departamento de MedicinaFunders
Junta de Comunidades de Castilla-La Mancha
Fundación de Investigación Médica Mutua Madrileña
Asociación Castellana de Aparato Digestivo
Bibliographic citation
World Journal of Gastroenterology, 2008, v. 14, n. 47, p. 7149-7159
Keywords
Chemokines
Hepatitis C virus
Persistent infection
Viral escape mechanism
Viral hepatitis pathogenesis
Description / Notes
11 p.
Project
info:eu-repo/grantAgreement/JCCM//PI-2007%32/ES//
info:eu-repo/grantAgreement/ACAD//ACAD%06/ES//
info:eu-repo/grantAgreement/FMM//2548%2008/ES//
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/publishedVersion
Rights
Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0)
Access rights
info:eu-repo/semantics/openAccess
Abstract
Chemokines produced in the liver during hepatitis C virus (HCV) infection induce migration of activated T cells from the periphery to infected parenchyma. The milieu of chemokines secreted by infected hepatocytes is predominantly associated with the T-helper/T-cytotoxic type-1 cell (Th1/Tc1) response. These chemokines consist of CCL3 (macrophage inflammatory protein-1?; MIP-1?), CCL4 (MIP- 1?) , CCL5 ( regulated on ac t ivat ion normal T cell expressed and secreted; RANTES), CXCL10 (interferon-??inducible protein-10; IP-10), CXCL11 (interferon-inducible T-cell ? chemoattractant; I-TAC), and CXCL9 (monokine induced by interferon ?; Mig) and they recruit T cells expressing either CCR5 or CXCR3 chemokine receptors. Intrahepatic and peripheral blood levels of these chemokines are increased during chronic hepatitis C. The interaction between chemokines and their receptors is essential in recruiting HCV-specific T cells to control the infection. When the adaptive immune response fails in this task, non-specific T cells without the capacity to control the infection are also recruited to the liver, and these are ultimately responsible for the persistent hepatic damage. The modulation of chemokine receptor expression and chemokine secretion could be a viral escape mechanism to avoid specific T cell migration to the liver during the early phase of infection, and to maintain liver viability during the chronic phase, by impairing non-specific T cell migration. Some chemokines and their receptors correlate with liver damage, and CXCL10 (IP-10) and CXCR3 levels have shown a clinical utility as predictors of treatment response outcome. The regulation of chemokines and their receptors could be a future potential therapeutic target to decrease liver inflammation and to increase specific T cell migration to the infected liver.
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