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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE44141 | GEO | 2013/05/03

SECONDARY ACCESSION(S): PRJNA188770

REPOSITORIES: GEO

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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

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

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

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

2013-03-07 | GSE41978 | GEO

Expression data from Id2-GFP- CDPs, Id2-GFP+ CDPs, Id2-GFP- pre-CD8, and Id2-GFP+ pre-CD8.

Project description:Expression data from Id2-GFP- CDPs, Id2-GFP+ CDPs, Id2-GFP- pre-CD8, and Id2-GFP+ pre-CD8.

| PRJNA509888 | ENA

Gene expression profiles in the embryonic midgut of Id2 knockout and wild-type mice

Project description:Id2 knockout mice develop heterotopic gastric tissues in the small intestine during development. To gain a mechanistic insight into the cell fate conversion in the Id2 knockout midgut endoderm, we performed microarray analysis using RNA samples extracted from midgut tissues at E13.5. We analyzed the gene expression patterns in the midgut of E13.5 Id2KO embryos compared to that of wild-type by microarrays.

2015-07-04 | E-GEOD-43014 | biostudies-arrayexpress

Gene expression profiles in the embryonic midgut of Id2 knockout and wild-type mice

2015-07-04 | GSE43014 | GEO

Opposing roles of E2A and Id3 that orchestrate and enforce the naive T cell fate

Project description:It is established that E2A and its antagonist, Id3, modulate developmental progression at the pre-TCR and TCR checkpoints. Here we show at a global scale how E2A promotes commitment to the T cell lineage and how pre-TCR mediated signalling affects E2A genome-wide occupancy. We find aberrant development of CD4 memory-like and TFH-like cells, T-B cell conjugates and, remarkably, B cell follicles in Id3-/-thymi. We also find that Id3-/-CD4 splenocytes exhibit increased numbers of TFH-like cells. We propose a model in which Id3 modulates the naive versus effector/memory cell fate. Collectively, these data show how E2A acts globally to orchestrate T-lineage development and that Id3 antagonizes E2A activity beyond the pre-TCR checkpoint to enforce the naive T cell fate. ChIP-Seq was performed in thymocytes isolated from either untreated Rag2-/-mice (DN3 cells) or Rag2-/- mice injected with anti-CD3e antibody (DN4 cells). ChIP used antibodies against either E2A or H3K4me1.

2011-07-31 | E-GEOD-30518 | biostudies-arrayexpress

ID2 controls differentiation of entero-endocrine cells in mouse small intestine

Project description:Aim: The mammalian gut is the largest endocrine organ. Dozens of hormones secreted by enteroendocrine cells regulate a variety of physiological functions of the gut but also of the pancreas and brain. Here, we examined the role of the helix-loop-helix transcription factor ID2 during the differentiation of intestinal stem cells along the enteroendocrine lineage. Methods: To assess the functions of ID2 in the adult mouse small intestine, we used single-cell RNA sequencing, genetically modified mice, and organoid assays. Results: We found that in the adult intestinal epithelium Id2 is predominantly expressed in enterochromaffin and peptidergic enteroendocrine cells. Consistently, the loss of Id2 leads to the reduction of Chromogranin A-positive enteroendocrine cells. In contrast, the numbers of tuft cells are increased in Id2 mutant small intestine. Moreover, ablation of Id2 elevates the numbers of Serotonin+ enterochromaffin cells and Ghrelin+ X-cells in the posterior part of the small intestine. Finally, Id2 acts downstream of BMP signalling during the differentiation of Glucagon Like Peptide-1+ L-cells and Cholecystokinin+ I-cells towards Neurotensin+PYY+ N-cells. Conclusion: Id2 plays an important role in cell fate decisions in the adult small intestine. Firstly, ID2 suppresses the differentiation of secretory intestinal epithelial progenitors towards tuft cell lineage and thus controls host immune response on commensal and parasitic microbiota. Next, ID2 is essential for establishing a differentiation gradient for enterochromaffin and X-cells along the anterior-posterior axis of the gut. Finally, ID2 is necessary for the differentiation of N-cells thus ensuring a differentiation gradient along the crypt-villi axis.

2022-06-21 | GSE178586 | GEO

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