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Gene-expression profile of Id2+ versus Id2KO KLRG1lo cells during infection

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.

ORGANISM(S): Mus musculus

PROVIDER: GSE41978 | GEO | 2013/03/07

SECONDARY ACCESSION(S): PRJNA178637

REPOSITORIES: GEO

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Gene-expression profile of Id2+ versus Id2KO KLRG1lo cells during infection

Project description: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. Gene-expression analysis of Wild-type, Id2KO, Id2KOBimKO and BimKO effector CD8+ cells on day 6 of Listeria infection. 2 or more replicates per sample were analyzed.

2013-03-07 | E-GEOD-41978 | biostudies-arrayexpress

Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

Project description:The transcription factor Inhibitor of DNA binding 2 (Id2) modulates T cell fate decisions but the molecular mechanism underpinning this regulation is unclear. Here, using whole genome mRNA analysis we show that loss of Id2 programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. Our findings reveal that the Id2-E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation. Wild-type and Id2fl/flLckCre+ DbNP366-specific CD8+ T cells were isolated from the spleen of PR8-primed/HKx31-infected Ly5.2+Id2fl/flLckCre+:Ly5.1+ mixed bone marrow chimeric mice ten days after intranasal influenza infection and analysed by whole genome mRNA analysis. Three biological replicates of each genotype were subjected to microarray analysis.

2013-05-03 | E-GEOD-44141 | biostudies-arrayexpress

Expression data from sorted Id3-GFP hi Id2-YFP int and Id3-GFP lo Id2-YFP hi activated CD8 T cells

Project description:During an immune response, CD8 T cells fall along a gradient of memory potential, but the regulators of these fate decsisions are not well understood. We utlized Id3-GFP and Id2-YFP reporter mice to elucidate the role of Id3 and Id2 during early CD8 T cell differentiation by gene expression. Id3-GFP hi Id2-YFP int or Id3-GFP lo Id2-YFP hi OT-I cells were sorted into trizol at day 6 of VSV-OVA infection and analyzed by microarray

2011-10-06 | E-GEOD-32675 | biostudies-arrayexpress

Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

2013-05-03 | GSE44141 | GEO

Whole genome mRNA analysis of virus-specific CD8+ T cells expressing different levels of Id2-GFP following influenza virus infection

Project description:We speculated that distinct levels of Id2 was deterministic in the transcriptional program of antigen-specific CD8+ T cells. To test this hypothesis, we subjected DbNP366-specific effector CD8+ T cells purified according to their differential expression of Id2-GFP (Id2-GFPint and Id2-GFPhigh) to microarray analysis and compared their gene expression profiles to the differentially expressed genes identified by comparing Id2-deficient and wild-type DbNP366-specific CD8+ T cells. This analysis revealed that the transcriptional program of CD8+ T cell differentiation is exquisitely sensitive to the concentration of Id2. PR8-primed Id2gfp/gfp mice were challenged after one month with influenza intranasally HKx31 virus and analysed on day 9 for the expression of Id2-GFP in DbNP366+CD44+ CD8+ T cells. DbNP366-specific CD8+ T cells were then separated into virus-specific CD8+ T cells that expressed intermediate or high levels of GFP. Purified Id2-GFPintermediate (int) and Id2-GFPhigh DbNP366-specific CD8+ T cells were analysed by mRNA whole genome microarray. Three replicates of each group (Id2-GFPint or Id2-GFPhigh) were analysed.

2013-05-03 | E-GEOD-44140 | biostudies-arrayexpress

Expression data from sorted Id3-GFP hi Id2-YFP int and Id3-GFP lo Id2-YFP hi activated CD8 T cells

2011-10-07 | GSE32675 | GEO

Id2-deficient NK cells acquire a naïve-like fate (Affymetrix data set)

Project description:All innate lymphoid cells (ILC) constitutively express and require the small helix-loop-helix protein ID2 but the functions of ID2 are not well understood in these cells. Here we show that natural killer (NK) cells, the prototypic ILC, can develop in the absence of ID2 but lose their innate properties and remain as CD27+CD11b- cells that fail to mature into cytotoxic effectors. We show that ID2 broadly limited chromatin accessibility at E protein binding sites near T lymphocyte-associated genes including multiple chemokine receptors, cytokine receptors, and signaling molecules. Moreover, ID2 prevented the conversion of CD27+CD11b- NK cells from a CD8 memory precursor-like chromatin accessibility state toward a naïve-like chromatin accessibility state, and altered their functional capacity. Finally, we demonstrate that increased expression of the naïve T cell-associated helix-loop-helix protein ID3 was required for development of ID2-deficient NK cells, indicating that completely unfettered E protein function is incompatible with NK cell development. These data solidify the roles of ID2 and ID3 as mediators of effector and naïve gene programs, respectively, and revealed a critical role for ID2 in promoting a chromatin state and transcriptional program in CD27+CD11b- NK cells that supports the innate properties of these cells and their ability to undergo cytotoxic effector differentiation.

2018-02-26 | GSE109456 | GEO

Whole genome mRNA analysis of virus-specific CD8+ T cells expressing different levels of Id2-GFP following influenza virus infection

2013-05-03 | GSE44140 | GEO

Id2-deficient NK cells acquire a naïve-like fate (ATAC-seq data set)

2018-02-26 | GSE109517 | GEO

Longitudinal expression data from CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD8+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-Db GP33-specific CD8+ T cells were sorted using MHC-I tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD8+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays

2012-11-23 | E-GEOD-41867 | biostudies-arrayexpress

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