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- W2016081852 startingPage "e1003422" @default.
- W2016081852 abstract "Loss of CD4 T cell help correlates with virus persistence during acute hepatitis C virus (HCV) infection, but the underlying mechanism(s) remain unknown. We developed a combined proliferation/intracellular cytokine staining assay to monitor expansion of HCV-specific CD4 T cells and helper cytokines expression patterns during acute infections with different outcomes. We demonstrate that acute resolving HCV is characterized by strong Th1/Th17 responses with specific expansion of IL-21-producing CD4 T cells and increased IL-21 levels in plasma. In contrast, viral persistence was associated with lower frequencies of IL-21-producing CD4 T cells, reduced proliferation and increased expression of the inhibitory receptors T cell immunoglobulin and mucin-domain-containing-molecule-3 (Tim-3), programmed death 1 (PD-1) and cytotoxic T-lymphocyte antigen 4 (CTLA-4) on HCV-specific CD8 T cells. Progression to persistent infection was accompanied by increased plasma levels of the Tim-3 ligand Galectin-9 (Gal-9) and expansion of Gal-9 expressing regulatory T cells (Tregs). In vitro supplementation of Tim-3(high) HCV-specific CD8 T cells with IL-21 enhanced their proliferation and prevented Gal-9 induced apoptosis. siRNA-mediated knockdown of Gal-9 in Treg cells rescued IL-21 production by HCV-specific CD4 T cells. We propose that failure of CD4 T cell help during acute HCV is partially due to an imbalance between Th17 and Treg cells whereby exhaustion of both CD4 and CD8 T cells through the Tim-3/Gal-9 pathway may be limited by IL-21 producing Th17 cells or enhanced by Gal-9 producing Tregs." @default.
- W2016081852 created "2016-06-24" @default.
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- W2016081852 creator A5061560140 @default.
- W2016081852 creator A5067087473 @default.
- W2016081852 date "2013-06-20" @default.
- W2016081852 modified "2023-10-17" @default.
- W2016081852 title "Galectin-9 and IL-21 Mediate Cross-regulation between Th17 and Treg Cells during Acute Hepatitis C" @default.
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- W2016081852 doi "https://doi.org/10.1371/journal.ppat.1003422" @default.
- W2016081852 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3688567" @default.
- W2016081852 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23818845" @default.
- W2016081852 hasPublicationYear "2013" @default.
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