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Systematic name M9560
Brief description Genes down-regulated in KLRG1 low [GeneID=10219] CD8 T effector cells during infection: ID2 [GeneID=3398] knockout versus ID2 and BCL2L11 [GeneID=3398;10018] knockout.
Full description or abstract CD8+ T cells play a crucial role in the clearance of intracellular pathogens through the generation of cytotoxic effector cells that eliminate infected cells and long-lived memory cells that provide enhanced protection against reinfection. We have previously shown that the inhibitor of E protein transcription factors, Id2, is necessary for accumulation of effector and memory CD8+ T cells during infection. Here we show that CD8+ T cells lacking Id2 did not generate a robust terminally-differentiated KLRG1hi effector population, but displayed a cell-surface phenotype and cytokine profile consistent with memory precursors, raising the question as to whether loss of Id2 impairs the differentiation and/or survival of effector-memory cells. We found that deletion of Bim rescued Id2-deficient CD8+ cell survival during infection. However, the dramatic reduction in KLRG1hi cells caused by loss of Id2 remained in the absence of Bim, such that Id2/Bim double-deficient cells form an exclusively KLRG1loCD127hi memory precursor population. Thus we describe a role for Id2 in both the survival and differentation of normal CD8+ effector and memory populations.
Collection C7: Immunologic Signature
      IMMUNESIGDB: ImmuneSigDB
Source publication Pubmed 23325888   Authors: Knell J,Best JA,Lind NA,Yang E,D'Cruz LM,Goldrath AW
Exact source GSE41978_3692_200_DN
Related gene sets (show 13 additional gene sets from the source publication)

(show 37 gene sets from the same authors)
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Organism Mus musculus
Contributed by Jernej Godec (Dana-Farber Cancer Institute)
Source platform HUMAN_GENE_SYMBOL
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Compendia expression profiles ? GTEx compendium
Human tissue compendium (Novartis)
Global Cancer Map (Broad Institute)
NCI-60 cell lines (National Cancer Institute)
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Version history 7.3: Moved to ImmuneSigDB sub-collection.

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