Journal
FRONTIERS IN IMMUNOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.607889
Keywords
GWAS; genome wide association screen; Itgae; CD103; vesicular stomatitis virus; IFN-I; AKT; mTOR
Categories
Funding
- Deutsche Forschungsgemeinschaft (DFG) [LA1419/7-1, LA1419/10-1, LA1558/5-1, 715 SI1558/3-1]
- Jurgen Manchot Foundation (MOI)
- FONDECYT [1180337]
- [Sonderforschungsbereich SFB974]
- [Transregio TRR60]
- [RTG1949/1]
- [RTG2098]
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In this study, CD103 was identified as a new regulator of antiviral IFN-I production in a mouse model of vesicular stomatitis virus (VSV) infection. CD103 specifically expressed by splenic conventional dendritic cells (cDCs) limited IFN-I production through suppressing AKT phosphorylation and mTOR activation in DCs during VSV infection, which accelerated early IFN-I in cDCs and prevented death in VSV infected animals.
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 (Itgae, 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.
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