Hepatitis C virus E2 envelope protein induces dendritic cell maturation

Zhou, Yonggang; Lukes, Yvonne; Anderson, Jonathan; Fileta, Bader B.; Reinhardt, Birgit; Sjögren, Maria H.

doi:10.1111/j.1365-2893.2007.00879.x

Cited by 16 publications

(12 citation statements)

References 48 publications

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“…Consistent with this model is the prior finding that that HCV E2 increases MoDC CD80, CD83, CD86, CD40, and major histocompatibility complex II expression (57). However, in contrast to results obtained by Zhou et al (57) that E2-matured MoDCs showed a greater capacity to stimulate T-cell proliferation, IFN-␥ production, and IL-12 production, we found an impaired mDC capacity to activate naive T cells.…”

Section: Discussioncontrasting

confidence: 57%

Differential Effects of Hepatitis C Virus JFH1 on Human Myeloid and Plasmacytoid Dendritic Cells

Liang¹,

Russell

Yonkers³

et al. 2009

J Virol

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Dendritic cells (DCs) are reported to be functionally deficient during chronic hepatitis C virus (HCV) infection.Differing results have been reported on direct effects of intact replicative-form HCV on DC function. To better understand the effect of HCV on DC function, we treated freshly purified human myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) with HCV JFH1. We found that HCV upregulated mDC maturation marker (CD83, CD86, and CD40) expression and did not inhibit Toll-like receptor 3 (TLR3) ligand [poly(I:C)]-induced mDC maturation, a finding consistent with the phenotype of DCs from HCV-infected subjects. At the same time, HCV JFH1 inhibited the ability of poly(I:C)-treated mDCs to activate naive CD4 T cells. In contrast, although there was no direct effect of virus on pDC maturation, HCV JFH1 inhibited TLR7 ligand (R848)-induced pDC CD40 expression, and this was associated with impaired ability to activate naive CD4 T cells. Parallel experiments with recombinant HCV proteins indicated HCV core protein may be responsible for a portion of the activity. Furthermore, HCV-mediated mDC maturation was dependent upon CD81-E2 interaction and, in part, TLR2. Using UV-treated HCV, we show that HCV-mediated mDC and pDC maturation is virus replication independent and, using strand specific PCR, we found no evidence for HCV replication within DCs. Because these effects of HCV on DC subset maturation and function in part recapitulate direct ex vivo analysis of DCs in chronic HCV infection, the mechanisms described here likely account for a portion of the DC subset defects observed in vivo.

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Section: Discussioncontrasting

confidence: 57%

Differential Effects of Hepatitis C Virus JFH1 on Human Myeloid and Plasmacytoid Dendritic Cells

Liang¹,

Russell

Yonkers³

et al. 2009

J Virol

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“…The inflammatory response is initiated by the presence of virus particles and subsequent infection of hepatocytes. Binding of microbial PAMPs, such as HCV glycoproteins, to antigen presenting cells results in activation and initiation of the inflammatory response and presentation of viral antigens to T cells [40,41,42,43,44,45]. Activation of these cells by viral proteins results in production of the soluble cytokines IL-1α, IL-1β and TNF-α, and the IL-6 family of cytokines, which in turn stimulate hepatocytes to produce acute‑phase proteins.…”

Section: Induction Of Acute Phase Proteins In Virus Infectionsmentioning

confidence: 99%

The Role of Humoral Innate Immunity in Hepatitis C Virus Infection

Tarr

Urbanowicz

Ball

2012

Viruses

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Infection with Hepatitis C Virus (HCV) causes chronic disease in approximately 80% of cases, resulting in chronic inflammation and cirrhosis. Current treatments are not completely effective, and a vaccine has yet to be developed. Spontaneous resolution of infection is associated with effective host adaptive immunity to HCV, including production of both HCV-specific T cells and neutralizing antibodies. However, the supporting role of soluble innate factors in protection against HCV is less well understood. The innate immune system provides an immediate line of defense against infections, triggering inflammation and playing a critical role in activating adaptive immunity. Innate immunity comprises both cellular and humoral components, the humoral arm consisting of pattern recognition molecules such as complement C1q, collectins and ficolins. These molecules activate the complement cascade, neutralize pathogens, and recruit antigen presenting cells. Here we review the current understanding of anti-viral components of the humoral innate immune system that play a similar role to antibodies, describing their role in immunity to HCV and their potential contribution to HCV pathogenesis.

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“…The HCV envelope glycoprotein E2 binding to DC was shown to lead to a shift from immature to mature phenotype through increased expression of cell surface molecules, such as CD83, CD80, CD11c, and MHC class II [142]. DCs that were E2-matured displayed a higher capacity to stimulate T cell proliferation and IFN-γ and IL-12 production in comparison to immature DCs.…”

Section: Hepatitis Viruses B and C And Dendritic Cellsmentioning

confidence: 99%

“…Moreover, E2-matured DCs showed a declined activity in endocytosis and phagocytosis upon maturation. Thus, the results indicate that E2 proteins not only induce DC maturation, but may also play a role in immune regulation during HCV infection [142]. Furthermore, DC migration appears to be significantly affected by interactions of HCV E2 with CD81 [128].…”

Section: Hepatitis Viruses B and C And Dendritic Cellsmentioning

confidence: 99%

The Tug-of-War between Dendritic Cells and Human Chronic Viruses

Rahman

Khan

Jain

2011

International Reviews of Immunology

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The human immune system is under constant challenge from many viruses, some of which the body is successfully able to clear. Other viruses have evolved to escape the host immune responses and thus persist, leading to the development of chronic diseases. Dendritic cells are professional antigen-presenting cells that play a major role in both innate and adaptive immunity against different pathogens. This review focuses on the interaction of different chronic viruses with dendritic cells and the viruses’ ability to exploit this critical cell type to their advantage so as to establish persistence within the host.

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Hepatitis C virus E2 envelope protein induces dendritic cell maturation

Cited by 16 publications

References 48 publications

Differential Effects of Hepatitis C Virus JFH1 on Human Myeloid and Plasmacytoid Dendritic Cells

Differential Effects of Hepatitis C Virus JFH1 on Human Myeloid and Plasmacytoid Dendritic Cells

The Role of Humoral Innate Immunity in Hepatitis C Virus Infection

The Tug-of-War between Dendritic Cells and Human Chronic Viruses

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