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Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [ATAC-Seq]

ABSTRACT: To investigate whether Id3 alters chromasome accessibility during CD4 T cell activation and Th1 differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE230082 | GEO | 2024/01/24

REPOSITORIES: GEO

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Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [RNA-Seq]

Project description:To comprehensively identify the transcriptional regulatory pathways by Id3 during CD4 T cell activation and Th1 differentiation.

2024-01-24 | GSE230274 | GEO

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [scRNA-Seq]

Project description:To identify how Id3 transcriptionaly regulate alloreactive CD4 T cells and whether this leads to the generation of distinct alloreactive donor T cell populations.

2024-01-24 | GSE230285 | GEO

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-24 | GSE230286 | GEO

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses

Project description:Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses

| PRJNA958187 | ENA

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [ATAC-Seq]

Project description:Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [ATAC-Seq]

| PRJNA957431 | ENA

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [scRNA-Seq]

Project description:Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [scRNA-Seq]

| PRJNA958198 | ENA

Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [RNA-Seq]

Project description:Id3 is required for the maintenance of tissue-infiltrating alloreactive T cells in GVHD but not anti-leukemia responses [RNA-Seq]

| PRJNA958172 | ENA

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

Identifying the role of ID3 in DNA repair and maintenance of genome integrity

Project description:The inhibitor of DNA-binding 3 (ID3) is a transcriptional repressor protein that limits the binding of basic helixÃ‚Âloop-helix (bHLH) transcription factors to DNA. Preliminary results from our lab confirm that cellular depletion of ID3 is associated with an impaired DNA damage response. we hypothesize that ID3 has the potential to epigenetically affect DNA repair. This is based on our observation that upon cellular ID3 knockdown, a reduction of chromatin-bound H4K16ac and H3K36me3.

| EGAS00001004478 | EGA

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

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