Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection

Ya-Lang Huang et al. report a mechanism for TLR3-mediated signaling after immune simulation and influenza virus infection by way of the co-receptor CLEC18A. This study found that a single amino acid change in CLEC18A(S339R) can enhance the production of type I and type III interferons to suppress vi...

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Autores principales: Ya-Lang Huang, Ming-Ting Huang, Pei-Shan Sung, Teh-Ying Chou, Ruey-Bing Yang, An-Suei Yang, Chung-Ming Yu, Yu-Wen Hsu, Wei-Chiao Chang, Shie-Liang Hsieh
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Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/6fa2f4a4e45c413fa7b217a06e675fd7
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spelling oai:doaj.org-article:6fa2f4a4e45c413fa7b217a06e675fd72021-12-02T12:11:51ZEndosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection10.1038/s42003-021-01745-72399-3642https://doaj.org/article/6fa2f4a4e45c413fa7b217a06e675fd72021-02-01T00:00:00Zhttps://doi.org/10.1038/s42003-021-01745-7https://doaj.org/toc/2399-3642Ya-Lang Huang et al. report a mechanism for TLR3-mediated signaling after immune simulation and influenza virus infection by way of the co-receptor CLEC18A. This study found that a single amino acid change in CLEC18A(S339R) can enhance the production of type I and type III interferons to suppress viral replication, and increase mice survival rate after flu infection infection.Ya-Lang HuangMing-Ting HuangPei-Shan SungTeh-Ying ChouRuey-Bing YangAn-Suei YangChung-Ming YuYu-Wen HsuWei-Chiao ChangShie-Liang HsiehNature PortfolioarticleBiology (General)QH301-705.5ENCommunications Biology, Vol 4, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Ya-Lang Huang
Ming-Ting Huang
Pei-Shan Sung
Teh-Ying Chou
Ruey-Bing Yang
An-Suei Yang
Chung-Ming Yu
Yu-Wen Hsu
Wei-Chiao Chang
Shie-Liang Hsieh
Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
description Ya-Lang Huang et al. report a mechanism for TLR3-mediated signaling after immune simulation and influenza virus infection by way of the co-receptor CLEC18A. This study found that a single amino acid change in CLEC18A(S339R) can enhance the production of type I and type III interferons to suppress viral replication, and increase mice survival rate after flu infection infection.
format article
author Ya-Lang Huang
Ming-Ting Huang
Pei-Shan Sung
Teh-Ying Chou
Ruey-Bing Yang
An-Suei Yang
Chung-Ming Yu
Yu-Wen Hsu
Wei-Chiao Chang
Shie-Liang Hsieh
author_facet Ya-Lang Huang
Ming-Ting Huang
Pei-Shan Sung
Teh-Ying Chou
Ruey-Bing Yang
An-Suei Yang
Chung-Ming Yu
Yu-Wen Hsu
Wei-Chiao Chang
Shie-Liang Hsieh
author_sort Ya-Lang Huang
title Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
title_short Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
title_full Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
title_fullStr Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
title_full_unstemmed Endosomal TLR3 co-receptor CLEC18A enhances host immune response to viral infection
title_sort endosomal tlr3 co-receptor clec18a enhances host immune response to viral infection
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/6fa2f4a4e45c413fa7b217a06e675fd7
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