NDLI: Dendritic cell inhibition is connected to exhaustion of CD8+ T cell polyfunctionality during chronic hepatitis C virus infection.

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Dendritic cell inhibition is connected to exhaustion of CD8+ T cell polyfunctionality during chronic hepatitis C virus infection.

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Dendritic cell inhibition is connected to exhaustion of CD8+ T cell polyfunctionality during chronic hepatitis C virus infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jouan, Loubna Willems, Bernard Rodrigue-Gervais, Ian Gaël Sékaly, Rafick-Pierre Rigsby, Hawley Sauvé, Dominike Lamarre, Daniel
Description	Country affiliation: Canada Author Affiliation: Rodrigue-Gervais IG ( Département de Microbiologie et Immunologie, Centre de Recherche du Centre Hospitalier de Université de Montréal, Montréal, Québec, Canada.)
Abstract	Although chronic viral infections have evolved mechanisms to interfere with aspects of pathogen recognition by dendritic cells (DCs), the role that these APCs play in virus-specific T cell exhaustion is unclear. Herein we report that NS3-dependent suppression of Toll/IL-1 domain-containing adapter-inducing IFN-beta- and IFN-beta promoter stimulator-1- but not MyD88-coupled pathogen-recognition receptor-induced synthesis of proinflammatory cytokines (IL-12 and TNF-alpha) from DCs by hepatitis C virus (HCV) is a distinctive feature of a subgroup of chronically infected patients. The result is decreased CD8(+) T cell polyfunctional capacities (production of IFN-gamma, IL-2, TNF-alpha, and CD107a mobilization) that is confined to HCV specificities and that relates to the extent to which HCV inhibits DC responses in infected subjects, despite comparable plasma viral load, helper T cell environments, and inhibitory programmed death 1 receptor/ligand signals. Thus, subjects in whom pathogen-recognition receptor signaling in DCs was intact exhibited enhanced polyfunctionality (i.e., IL-2-secretion and CD107a). In addition, differences between HCV-infected patients in the ability of CD8(+) T cells to activate multiple functions in response to HCV did not apply to CD8(+) T cells specific for other immune-controlled viruses (CMV, EBV, and influenza). Our findings identify reversible virus evasion of DC-mediated innate immunity as an additional important factor that impacts the severity of polyfunctional CD8(+) T cell exhaustion during a chronic viral infection.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	6
Volume Number	184
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-03-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Virology Dendritic Cells Hepacivirus Hepatitis C, Chronic Immunosuppression Antigens, Surface Physiology Apoptosis Regulatory Proteins Pathology Cell Degranulation Interleukin-2 Biosynthesis Longitudinal Studies Myeloid Cells Programmed Cell Death 1 Receptor Receptors, Pattern Recognition Antagonists & Inhibitors Viral Load Virus Activation Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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