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Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation

Zika virus (ZIKV) is a mosquito-borne pathogen with increasing public health significance. To characterize immune responses to ZIKV, here we examine transcriptional signatures of CD4 T, CD8 T, B, and NK cells, monocytes, myeloid dendritic cells (mDCs), and plasmacytoid dendritic cells (pDCs) from th...

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Autores principales: Sun, Xiaoming, Hua, Stephane, Gao, Ce, Blackmer, Jane E., Ouyang, Zhengyu, Ard, Kevin, Ciaranello, Andrea, Yawetz, Sigal, Sax, Paul E., Rosenberg, Eric S., Lichterfeld, Mathias, Yu, Xu G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7229207/
https://www.ncbi.nlm.nih.gov/pubmed/32415086
http://dx.doi.org/10.1038/s41467-020-16217-5
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author Sun, Xiaoming
Hua, Stephane
Gao, Ce
Blackmer, Jane E.
Ouyang, Zhengyu
Ard, Kevin
Ciaranello, Andrea
Yawetz, Sigal
Sax, Paul E.
Rosenberg, Eric S.
Lichterfeld, Mathias
Yu, Xu G.
author_facet Sun, Xiaoming
Hua, Stephane
Gao, Ce
Blackmer, Jane E.
Ouyang, Zhengyu
Ard, Kevin
Ciaranello, Andrea
Yawetz, Sigal
Sax, Paul E.
Rosenberg, Eric S.
Lichterfeld, Mathias
Yu, Xu G.
author_sort Sun, Xiaoming
collection PubMed
description Zika virus (ZIKV) is a mosquito-borne pathogen with increasing public health significance. To characterize immune responses to ZIKV, here we examine transcriptional signatures of CD4 T, CD8 T, B, and NK cells, monocytes, myeloid dendritic cells (mDCs), and plasmacytoid dendritic cells (pDCs) from three individuals with ZIKV infection. While gene expression patterns from most cell subsets display signs of impaired antiviral immune activity, pDCs from infected host have distinct transcriptional response associated with activation of innate immune recognition and type I interferon signaling pathways, but downregulation of key host factors known to support ZIKV replication steps; meanwhile, pDCs exhibit a unique expression pattern of gene modules that are correlated with alternative cell populations, suggesting collaborative interactions between pDCs and other immune cells, particularly B cells. Together, these results point towards a discrete but integrative function of pDCs in the human immune responses to ZIKV infection.
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spelling pubmed-72292072020-06-05 Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation Sun, Xiaoming Hua, Stephane Gao, Ce Blackmer, Jane E. Ouyang, Zhengyu Ard, Kevin Ciaranello, Andrea Yawetz, Sigal Sax, Paul E. Rosenberg, Eric S. Lichterfeld, Mathias Yu, Xu G. Nat Commun Article Zika virus (ZIKV) is a mosquito-borne pathogen with increasing public health significance. To characterize immune responses to ZIKV, here we examine transcriptional signatures of CD4 T, CD8 T, B, and NK cells, monocytes, myeloid dendritic cells (mDCs), and plasmacytoid dendritic cells (pDCs) from three individuals with ZIKV infection. While gene expression patterns from most cell subsets display signs of impaired antiviral immune activity, pDCs from infected host have distinct transcriptional response associated with activation of innate immune recognition and type I interferon signaling pathways, but downregulation of key host factors known to support ZIKV replication steps; meanwhile, pDCs exhibit a unique expression pattern of gene modules that are correlated with alternative cell populations, suggesting collaborative interactions between pDCs and other immune cells, particularly B cells. Together, these results point towards a discrete but integrative function of pDCs in the human immune responses to ZIKV infection. Nature Publishing Group UK 2020-05-15 /pmc/articles/PMC7229207/ /pubmed/32415086 http://dx.doi.org/10.1038/s41467-020-16217-5 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Sun, Xiaoming
Hua, Stephane
Gao, Ce
Blackmer, Jane E.
Ouyang, Zhengyu
Ard, Kevin
Ciaranello, Andrea
Yawetz, Sigal
Sax, Paul E.
Rosenberg, Eric S.
Lichterfeld, Mathias
Yu, Xu G.
Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title_full Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title_fullStr Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title_full_unstemmed Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title_short Immune-profiling of ZIKV-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
title_sort immune-profiling of zikv-infected patients identifies a distinct function of plasmacytoid dendritic cells for immune cross-regulation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7229207/
https://www.ncbi.nlm.nih.gov/pubmed/32415086
http://dx.doi.org/10.1038/s41467-020-16217-5
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