整合素αE（CD103）限制常规树突状细胞中病毒诱导的I型干扰素产生。
Integrin Alpha E (CD103) Limits Virus-Induced IFN-I Production in Conventional Dendritic Cells.
作者信息
Duhan Vikas, Khairnar Vishal, Kitanovski Simo, Hamdan Thamer A, Klein Andrés D, Lang Judith, Ali Murtaza, Adomati Tom, Bhat Hilal, Friedrich Sarah-Kim, Li Fanghui, Krebs Philippe, Futerman Anthony H, Addo Marylyn M, Hardt Cornelia, Hoffmann Daniel, Lang Philipp A, Lang Karl S
机构信息
Institute of Immunology, Medical Faculty, University of Duisburg-Essen, Essen, Germany.
Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
出版信息
Front Immunol. 2021 Jan 27;11:607889. doi: 10.3389/fimmu.2020.607889. eCollection 2020.
Early and strong production of IFN-I by dendritic cells is important to control vesicular stomatitis virus (VSV), however mechanisms which explain this cell-type specific innate immune activation remain to be defined. Here, using a genome wide association study (GWAS), we identified Integrin alpha-E (, CD103) as a new regulator of antiviral IFN-I production in a mouse model of vesicular stomatitis virus (VSV) infection. CD103 was specifically expressed by splenic conventional dendritic cells (cDCs) and limited IFN-I production in these cells during VSV infection. Mechanistically, CD103 suppressed AKT phosphorylation and mTOR activation in DCs. Deficiency in CD103 accelerated early IFN-I in cDCs and prevented death in VSV infected animals. In conclusion, CD103 participates in regulation of cDC specific IFN-I induction and thereby influences immune activation after VSV infection.
树突状细胞早期大量产生I型干扰素（IFN-I）对于控制水疱性口炎病毒（VSV）至关重要，然而，解释这种细胞类型特异性先天免疫激活的机制仍有待确定。在此，我们利用全基因组关联研究（GWAS），在水疱性口炎病毒（VSV）感染的小鼠模型中，将整合素α-E（CD103）鉴定为抗病毒IFN-I产生的新调节因子。CD103在脾脏传统树突状细胞（cDCs）中特异性表达，并在VSV感染期间限制这些细胞中的IFN-I产生。从机制上讲，CD103抑制DCs中的AKT磷酸化和mTOR激活。CD103缺陷加速了cDCs中早期IFN-I的产生，并防止VSV感染动物死亡。总之，CD103参与cDC特异性IFN-I诱导的调节，从而影响VSV感染后的免疫激活。
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