Hepatitis C Virus E2 Envelope Glycoprotein Induces an Immunoregulatory Phenotype in Macrophages

Kwon, Young‐Chan; Meyer, Keith; Peng, Guangyong; Chatterjee, S.; Hoft, Daniel F.; Ray, Ranjit

doi:10.1002/hep.29843

Cited by 26 publications

(28 citation statements)

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“…The complement system is a group of proteins that works for the innate and adaptive immune responses. Complements play a role in inflammation by promoting dendritic cell (DC)‐mediated NK cell activation . Complement receptor gC1qR (receptor for the complement component C1q) expression on CD4 + T cells influences the outcome of HCV infection .…”

Section: Innate Immune Response To Hcv Infectionmentioning

confidence: 99%

“…Serum C3 level is depleted in HCV‐infected patients with cirrhosis. HCV E2 envelope glycoprotein suppresses C3 expression and impairs macrophage and DC maturation for antigen presentation and CD4 + T cell stimulation …”

Section: Innate Immune Response To Hcv Infectionmentioning

confidence: 99%

“…Complements play a role in inflammation by promoting dendritic cell (DC)-mediated NK cell activation. (35)(36)(37) Complement receptor gC1qR (receptor for the complement component C1q) expression on CD4 + T cells influences the outcome of HCV infection. (34) The frequency of gC1qR + CD4 + T cells increases and maintains during HCV infection, whereas this does not occur in individuals resolving HCV infection.…”

Section: Complement Regulationmentioning

confidence: 99%

“…HCV E2 envelope glycoprotein suppresses C3 expression and impairs macrophage and DC maturation for antigen presentation and CD4 + T cell stimulation. (37,38) HCV induces CD55 as a negative regulator of complement activation and suppresses C3, C4, and C9 complement components of the membrane attack complex. Up-regulation of CD55 expression on the cell surface or secretion by HCV core protein inhibits complement-dependent cytolysis.…”

Section: Complement Regulationmentioning

confidence: 99%

“…HCV E2 induces immune regulatory cytokine IL-10 and CD163 protein expression and enhances STAT3 and suppresses STAT1 activation in macrophages, suggesting the possibility for macrophage polarization toward the M2 phenotype. (37) Furthermore, E2 suppresses C3 complement expression, suggesting potential for impairment of immune cell priming. E2-associated macrophage polarization depends on the interaction with CD81 for epidermal growth factor receptor activation.…”

Section: Vaccine Developmentmentioning

confidence: 99%

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Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

Ray

2019

Hepatology

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Chronic hepatitis C virus (HCV) infection associated liver disease is a global health problem. HCV often causes silent disease, and eventually progresses to end stage liver disease. HCV infects hepatocytes, however initial manifestation of liver disease is mostly displayed in hepatic stellate cells causing fibrosis/cirrhosis, and believed to be occurring from inflammation in the liver. It is still unclear why HCV is not spontaneously cleared from infected liver in the majority of individuals and develops chronic infection with progressive liver disease. Direct-acting antivirals (DAAs) show excellent results in controlling viremia, although beneficial consequence in advanced liver disease remains to be understood. In this review, we highlight the current knowledge that has contributed in our understanding on the role of HCV in inflammation, immune evasion, metabolic disorders, liver pathogeneses, and efforts in vaccine development. This article is protected by copyright. All rights reserved.

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Section: Innate Immune Response To Hcv Infectionmentioning

confidence: 99%

Section: Innate Immune Response To Hcv Infectionmentioning

confidence: 99%

Section: Complement Regulationmentioning

confidence: 99%

Section: Complement Regulationmentioning

confidence: 99%

Section: Vaccine Developmentmentioning

confidence: 99%

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Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

Ray

2019

Hepatology

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Hepatitis C

Kanto

Yoshio

2020

Liver Immunology

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Macrophage subsets and their role: co-relation with colony-stimulating factor-1 receptor and clinical relevance

et al. 2022

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Macrophages are one of the first innate immune cells to reach the site of infection or injury. Diverse functions from the uptake of pathogen or antigen, its killing, and presentation, the release of pro- or anti-inflammatory cytokines, activation of adaptive immune cells, clearing off tissue debris, tissue repair, and maintenance of tissue homeostasis have been attributed to macrophages. Besides tissue-resident macrophages, the circulating macrophages are recruited to different tissues to get activated. These are highly plastic cells, showing a spectrum of phenotypes depending on the stimulus received from their immediate environment. The macrophage differentiation requires colony-stimulating factor-1 (CSF-1) or macrophage colony-stimulating factor (M-CSF), colony-stimulating factor-2 (CSF-2), or granulocyte–macrophage colony-stimulating factor (GM-CSF) and different stimuli activate them to different phenotypes. The richness of tissue macrophages is precisely controlled via the CSF-1 and CSF-1R axis. In this review, we have given an overview of macrophage origin via hematopoiesis/myelopoiesis, different phenotypes associated with macrophages, their clinical significance, and how they are altered in various diseases. We have specifically focused on the function of CSF-1/CSF-1R signaling in deciding macrophage fate and the outcome of aberrant CSF-1R signaling in relation to macrophage phenotype in different diseases. We further extend the review to briefly discuss the possible strategies to manipulate CSF-1R and its signaling with the recent updates. Graphical Abstract

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Hepatitis C Virus E2 Envelope Glycoprotein Induces an Immunoregulatory Phenotype in Macrophages

Abstract: Our results suggest that E2 EnvGP may not be an ideal candidate for HCV vaccine development, and discrete domains within E2 may prove to be more capable of elliciting a protective immune response. (Hepatology 2018).

Cited by 26 publications

References 50 publications

Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

Hepatitis C

Macrophage subsets and their role: co-relation with colony-stimulating factor-1 receptor and clinical relevance

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