Role of A20 in interferon‐α‐mediated functional restoration of myeloid dendritic cells in patients with chronic hepatitis C
Summary Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon‐α (IFN‐α) ‐based antiviral therapies; howeve...
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| Published in | Immunology Vol. 143; no. 4; pp. 670 - 678 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BlackWell Publishing Ltd
01.12.2014
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0019-2805 1365-2567 1365-2567 |
| DOI | 10.1111/imm.12350 |
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| Abstract | Summary
Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon‐α (IFN‐α) ‐based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN‐α treatment are unclear. The ubiquitin‐editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN‐α therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV‐infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN‐α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN‐α in vitro. Additionally, A20 expression by polyI:C‐activated mDCs, with or without IFN‐α treatment, negatively correlated with the expression of HLA‐DR, CD86 and CCR7, and the secretion of interleukin‐12 (IL‐12), but positively associated with the production of IL‐10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL‐12 in mDCs of chronically HCV‐infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. |
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| AbstractList | Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon-
α
(IFN-
α
) -based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN-
α
treatment are unclear. The ubiquitin-editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN-
α
therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV-infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN-
α
treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN-
α in vitro
. Additionally, A20 expression by polyI:C-activated mDCs, with or without IFN-
α
treatment, negatively correlated with the expression of HLA-DR, CD86 and CCR7, and the secretion of interleukin-12 (IL-12), but positively associated with the production of IL-10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL-12 in mDCs of chronically HCV-infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon-α (IFN-α) -based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN-α treatment are unclear. The ubiquitin-editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN-α therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV-infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN-α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN-α in vitro. Additionally, A20 expression by polyI:C-activated mDCs, with or without IFN-α treatment, negatively correlated with the expression of HLA-DR, CD86 and CCR7, and the secretion of interleukin-12 (IL-12), but positively associated with the production of IL-10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL-12 in mDCs of chronically HCV-infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection.Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon-α (IFN-α) -based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN-α treatment are unclear. The ubiquitin-editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN-α therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV-infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN-α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN-α in vitro. Additionally, A20 expression by polyI:C-activated mDCs, with or without IFN-α treatment, negatively correlated with the expression of HLA-DR, CD86 and CCR7, and the secretion of interleukin-12 (IL-12), but positively associated with the production of IL-10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL-12 in mDCs of chronically HCV-infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon-α (IFN-α) -based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN-α treatment are unclear. The ubiquitin-editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN-α therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV-infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN-α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN-α in vitro. Additionally, A20 expression by polyI:C-activated mDCs, with or without IFN-α treatment, negatively correlated with the expression of HLA-DR, CD86 and CCR7, and the secretion of interleukin-12 (IL-12), but positively associated with the production of IL-10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL-12 in mDCs of chronically HCV-infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. Hepatitis C virus ( HCV ) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells ( mDC s). This defect appears to be remedied by treatment with interferon‐ α ( IFN ‐ α ) ‐based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN ‐ α treatment are unclear. The ubiquitin‐editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDC s. We propose that the expression of A20 correlates with the function of mDC s during HCV infection and IFN ‐ α therapy. In this study, we observed that A20 expression in mDC s isolated from chronically HCV ‐infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses ( SVR ) following antiviral treatment. Notably, A20 expression in mDC s from HCV patients during IFN ‐ α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDC s stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN ‐ α in vitro . Additionally, A20 expression by polyI:C‐activated mDC s, with or without IFN ‐ α treatment, negatively correlated with the expression of HLA ‐ DR , CD 86 and CC R7, and the secretion of interleukin‐12 ( IL ‐12), but positively associated with the production of IL ‐10. Importantly, silencing A20 expression using small interfering RNA s increased the production of IL ‐12 in mDC s of chronically HCV ‐infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. Summary Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon‐α (IFN‐α) ‐based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN‐α treatment are unclear. The ubiquitin‐editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs. We propose that the expression of A20 correlates with the function of mDCs during HCV infection and IFN‐α therapy. In this study, we observed that A20 expression in mDCs isolated from chronically HCV‐infected subjects was significantly higher than healthy subjects or subjects achieving sustained virological responses (SVR) following antiviral treatment. Notably, A20 expression in mDCs from HCV patients during IFN‐α treatment was significantly lower than for untreated patients, SVR patients, or healthy subjects. Besides, A20 expression in mDCs stimulated by polyI:C differed between HCV patients and healthy subjects, and this difference could be abrogated by the treatment with IFN‐α in vitro. Additionally, A20 expression by polyI:C‐activated mDCs, with or without IFN‐α treatment, negatively correlated with the expression of HLA‐DR, CD86 and CCR7, and the secretion of interleukin‐12 (IL‐12), but positively associated with the production of IL‐10. Importantly, silencing A20 expression using small interfering RNAs increased the production of IL‐12 in mDCs of chronically HCV‐infected individuals. These findings suggest that A20 plays a crucial role in negative regulation of innate immune responses during chronic viral infection. |
| Author | Wang, Jiuping Zhou, Yongxing Moorman, Jonathan P. Yao, Zhi Q. Hao, Chunqiu He, Yu Guo, Yonghong Li, Yuan Ma, Li Zhou, Yun Zhang, Ying Jia, Zhansheng Lian, Jianqi |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24965710$$D View this record in MEDLINE/PubMed |
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| Keywords | hepatitis C virus myeloid dendritic cells interferon-α chronic infection A20 |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Li Ma and Yun Zhou contributed equally to this work and share first authorship on this study. Senior author: Yongxing Zhou |
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Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in... Hepatitis C virus ( HCV ) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in... Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid... |
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| SubjectTerms | A20 Adolescent Adult B7-2 Antigen - genetics B7-2 Antigen - metabolism Case-Control Studies chronic infection Dendritic Cells - drug effects Dendritic Cells - immunology Dendritic Cells - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Female Gene Expression Regulation - drug effects Genotype Hepacivirus - genetics Hepacivirus - immunology hepatitis C virus Hepatitis C, Chronic - drug therapy Hepatitis C, Chronic - genetics Hepatitis C, Chronic - immunology Hepatitis C, Chronic - metabolism Hepatitis C, Chronic - virology HLA-DR Antigens - genetics HLA-DR Antigens - metabolism Humans Interferon-alpha - metabolism Interferon-alpha - pharmacology Interferon-alpha - therapeutic use interferon‐α Interleukin-10 - biosynthesis Interleukin-12 - biosynthesis Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Male Middle Aged myeloid dendritic cells Nuclear Proteins - genetics Nuclear Proteins - metabolism Original Receptors, CCR7 - genetics Receptors, CCR7 - metabolism RNA, Messenger - genetics Tumor Necrosis Factor alpha-Induced Protein 3 Viral Load Young Adult |
| Title | Role of A20 in interferon‐α‐mediated functional restoration of myeloid dendritic cells in patients with chronic hepatitis C |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fimm.12350 https://www.ncbi.nlm.nih.gov/pubmed/24965710 https://www.proquest.com/docview/1623292419 https://pubmed.ncbi.nlm.nih.gov/PMC4253515 |
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