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Expression data analyzing ID3 (Inhibitor of DNA binding 3)-affected mouse T cells

ABSTRACT: Mouse CD8+ T cells affected by ID3 (Inhibitor of DNA binding 3) display patterns of gene expression suggesting enhanced persistance and survival. In this study, we identified genes differentially expressed between ID32a transduced and mock transduced, and ID32a knockout and wild type mouse CD8+ T cells. Most prominent functions of differentially expressed genes include DNA replication-associated repair, maintenance of chromosome stability and mitotic cell divison machinery. Overall, these data suggest that ID3 acts in favor of maintained survival in CD8+ mouse T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE23568 | GEO | 2011/10/16

SECONDARY ACCESSION(S): PRJNA130931

REPOSITORIES: GEO

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Expression data analyzing ID3 (Inhibitor of DNA binding 3)-affected mouse T cells

Project description:Mouse CD8+ T cells affected by ID3 (Inhibitor of DNA binding 3) display patterns of gene expression suggesting enhanced persistance and survival. In this study, we identified genes differentially expressed between ID32a transduced and mock transduced, and ID32a knockout and wild type mouse CD8+ T cells. Most prominent functions of differentially expressed genes include DNA replication-associated repair, maintenance of chromosome stability and mitotic cell divison machinery. Overall, these data suggest that ID3 acts in favor of maintained survival in CD8+ mouse T cells. Two independent microarray experiments were carried out using separate array batches, one comparing Id32aThy1.1 (ID32a transduced) with Thy1.1 pmel-1 (mock transduced) CD8+ T cells sorted 5 days after infection, and a second experiment comparing Id32a-/- (Id32a knockout)CD8+ T cells with Id32a+/+ (Id32a wild type) controls, both in an upaired design. Individual array samples were generated by pooling equal amounts of total RNA derived from purified T cells of four individual mice. Each experimental group consisted of four such microarrays (statistical group size n=4, pooled samples derived from 16 mice per assay group total).

2011-10-15 | E-GEOD-23568 | 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

Dynamic expression of Id3 defines the stepwise differentiation of tissue-resident regulatory T cells

Project description:Foxp3+ regulatory T (TR) cells are phenotypically and functionally diverse, and broadly distributed in lymphoid and non-lymphoid tissues. However, the pathways guiding the differentiation of tissue-resident TR populations have not been well defined. By regulating E-protein function, Id3 controls the differentiation of CD8+ effector T cells and is essential for TR maintenance and function. We show that dynamic expression of Id3 helps define three distinct mouse TR populations, Id3+CD62LhiCD44lo central (c)TR, Id3+CD62LloCD44hi effector (e)TR and Id3- eTR. Adoptive transfer experiments and transcriptome analyses support a stepwise model of differentiation from Id3+ cTR to Id3+ eTR to Id3- eTR. Furthermore, Id3- eTR have high expression of functional inhibitory markers and a transcriptional signature of tissue-resident TR. Accordingly, Id3- eTR are highly enriched in non-lymphoid organs, but virtually absent from blood and lymph. Thus, we propose that tissue-resident TR develop in a multi-step process associated with Id3 downregulation.

2018-11-16 | GSE122593 | GEO

The nuclear factor ID3 endows macrophages with a potent anti-tumor activity

Project description:Macrophage activation is controlled by a balance between activating and inhibitory receptors which protect normal tissues from excessive damage during infection but promote tumor growth and metastasis in cancer. We report here that the Kupffer cell (KC)-lineage determining factor ID3 controls this balance and selectively endows KC with the ability to phagocytose live tumor cells and orchestrate the recruitment, proliferation, and activation of NK and CD8 T lymphoid effector cells in the liver to restrict the growth of a variety of tumors. ID3 shifts the macrophage inhibitory/activating receptor balance to unleash the phagocytic and lymphoid response, at least in part by buffering binding of the transcription factors ELK1 and E2A at the Sirpα locus. Furthermore, loss- and gain-of-function experiments demonstrate that ID3 is sufficient to confer this potent anti-tumor activity to mouse bone marrow derived macrophages and human induced pluripotent stem cells derived macrophages. Expression of ID3 is therefore necessary and sufficient to endow macrophages with the ability to form an efficient anti-tumor niche, which could be harnessed for cell therapy in cancer.

2023-11-14 | GSE234638 | GEO

Id3 Orchestrates Germinal Center B Cell Development

Project description:Previous studies have demonstrated that E-proteins induce AID expression in activated B cells. Here we have examined the role of Id3 in germinal center (GC) cells. We found that Id3 expression is high in follicular B-lineage cells but declines in GC cells. Immunized mice depleted for Id3 expression displayed a block in germinal center B cell maturation, showed reduced numbers of marginal zone B cells and class switched cells, were associated with decreased antibody titers and lower numbers of plasma cells. In vitro Id3-depleted B cells displayed a defect in class switch recombination. Whereas AID levels were not altered in Id3-depleted activated B cells, the expression of a subset of genes encoding for signaling components of antigen receptor, cytokine receptor and chemokine receptor mediated signaling was significantly impaired. We propose that during the GC reaction Id3 levels decline to activate the expression of genes encoding for signaling components that mediate B cell receptor and or cytokine-mediated signaling to promote the differentiation of GC B cells.

2016-08-18 | GSE84374 | GEO

Gene expression profiles after induced Id3 levels in A431 squamous carcinoma cells

2015-06-30 | GSE64535 | GEO

Gene expression profiles after induced Id3 levels in A431 squamous carcinoma cells

Project description:Previously it has been shown that Id3 can act as an apoptosis-inducer gene in immortalized human keratinocytes. To further investigate the role of Id3 in the progression of skin cancer, the role of Id3 in A431 cells is investigated through ectopic induction of Id3. Microarray analysis is used to guide us the genes and pathways that are significantly altered after Id3 induction. 4 groups are included in this study, each with one sample. There are two cell lines: A431 cells stably transfected with Id3 or control vector. In each cell line, there are two conditions: induced and un-induced with tetracycline.

2015-06-30 | E-GEOD-64535 | biostudies-arrayexpress

ID3 Promotes Homologous Recombination via Non-transcriptional and Transcriptional Mechanisms and its Loss Confers Sensitivity to PARP Inhibition

Project description:The inhibitor of DNA-binding 3 (ID3) is a transcriptional regulator that limits interaction of basic helix-loop-helix transcription factors with their target DNA sequences. We previously reported that ID3 loss is associated with mutational signatures linked to DNA repair defects. Here we demonstrate that ID3 exhibits a dual role to promote DNA double-strand break (DSB) repair, particularly homologous recombination (HR). ID3 interacts with the MRN complex and RECQL helicase to activate DSB repair and it facilitates RAD51 loading and downstream steps of HR. In addition, ID3 promotes the expression of HR genes in response to ionizing radiation by regulating both chromatin accessibility and activity of the transcription factor E2F1. Consistently, analyses of TCGA cancer patient data demonstrate that low ID3 expression is associated with impaired HR. The loss of ID3 leads to sensitivity of tumor cells to PARP inhibition, offering new therapeutic opportunities in ID3-deficient tumors.

2022-02-17 | PXD028946 | Pride

Id2 and Id3 maintain the regulatory T cell pool to suppress inflammatory disease

Project description:Regulatory T (Treg) cells suppress the development of inflammatory disease, but our knowledge of transcriptional regulators that control this function remains incomplete. Here we show that expression of Id2 and Id3 in Treg cells was required to suppress development of fatal inflammatory disease. We found that T cell antigen receptor (TCR)-driven signaling initially decreased the abundance of Id3, which led to the activation of a follicular regulatory T (TFR) cell–specific transcription signature. However, sustained lower abundance of Id2 and Id3 interfered with proper development of TFR cells. Depletion of Id2 and Id3 expression in Treg cells resulted in compromised maintenance and localization of the Treg cell population. Thus, Id2 and Id3 enforce TFR cell checkpoints and control the maintenance and homing of Treg cells. Treg mRNA profiles in lymph node from 3-week-old Id2fl/flId3fl/fl;Foxp3Cre/Cre (Id2 Id3 double-knockout) and control mice are generated by deep sequencing.

2014-06-29 | E-GEOD-57682 | biostudies-arrayexpress

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