Transcriptomics

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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).

ORGANISM(S): Mus musculus

PROVIDER: GSE62729 | GEO | 2015/04/24

SECONDARY ACCESSION(S): PRJNA265051

REPOSITORIES: GEO

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