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
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/6fa2f4a4e45c413fa7b217a06e675fd7
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Sumario: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.