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Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

ABSTRACT: Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6). This study includes data from the spleen BALB/c mice, under steady-state or MCMV condition at different time points. 2 to 5 mice for each mouse strain for each time point were used, and were hybridized on 5 separate batches of gene chips.

ORGANISM(S): Mus musculus

SUBMITTER: Marc DALOD

PROVIDER: E-GEOD-62729 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6).

2015-04-24 | GSE62729 | GEO

Dissecting cell-intrinsic roles of MyD88 and IFN-I signalling in pDC responses to a viral infection in vivo

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I interferons (IFN-I) during viral infections, in response to triggering of endosomal Toll Like Receptors (TLR) 7 or 9 by viral single-stranded RNA or unmethylated CpG DNA, respectively. IFN-I production in pDC occurs in specialized endosomes encompassing preformed signaling complexes of TLR7 or 9 with their adaptor molecule MyD88 and the transcription factor interferon regulatory factor 7 (IRF7). The triggering of TLR leads to IRF7 phosphorylation, nuclear translocation and binding to the promoters of the genes encoding IFN-I to initiate their transcription. pDC express uniquely high levels of IRF7 at steady state and this expression is further enhanced by positive IFN-I feedback signaling during viral infections. However, the specific cell-intrinsic roles of MyD88 versus IFN-I signaling in pDC responses to a viral infection have not been rigorously dissected. To achieve this aim, we generated mixed bone marrow chimera mice (MBMC) allowing to rigorously compare the gene expression profiles of WT versus Ifnar1-KO or MyD88-KO pDC isolated from the same animals at steady state or after infection with the mouse cytomegalovirus (MCMV). Our results indicate that, in vivo during MCMV infection, pDC undergo a major transcriptional reprogramming, under combined instruction of IFN-I, IFN-γ and direct TLR triggering. However, these different stimuli drive specific, largely distinct, gene expression programs. We rigorously determined which gene modules require cell-intrinsic IFN-I signaling for their induction in pDC during a physiological viral infection in vivo. We delineated non-redundant versus shared versus antagonistic responses with IFN-γ. We demonstrated that cell-intrinsic IFN-I responsiveness is dispensable for induction of the expression of all IFN-I/III genes and many cytokines or chemokines in pDC during MCMV infection, contrary to MyD88 signaling.

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Dissecting the molecular programs governing interferon production by plasmacytoid dendritic cells during a viral infection in vivo

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A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

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A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

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2020-07-07 | GSE151244 | GEO

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