Frontiers in immunology · 2021
Integrin Alpha E (CD103) Limits Virus-Induced IFN-I Production in Conventional Dendritic Cells.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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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
Аннотация
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.
Предметные рубрики MeSH
AnimalsAntigens, CDCells, CulturedDendritic CellsDisease Models, AnimalGenome-Wide Association StudyHost-Pathogen InteractionsImmunity, InnateIntegrin alpha ChainsInterferon Type IMice, 129 StrainMice, Inbred AKRMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, Inbred DBAMice, Inbred NODMice, KnockoutPhosphorylationProto-Oncogene Proteins c-aktReceptor, Interferon alpha-betaSignal TransductionTOR Serine-Threonine KinasesVesicular StomatitisVesiculovirusVirus ReplicationMice