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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE230285 | 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 [ATAC-Seq]

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

2024-01-24 | GSE230082 | GEO

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: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

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 [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

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

Tissue-Resident Memory T Cells in Human Kidney Transplants have alloreactive potential

Project description:The extent to which tissue-resident memory T (TRM) cells in transplanted organs possess alloreactivity is uncertain. This study investigates the alloreactive potential of TRM cells in kidney explants from four patients who experienced severe acute rejection leading to graft loss. Alloreactive T-cell receptors (TCRs) clones were identified in pre-transplant blood samples through mixed lymphocyte reactions, followed by single-cell RNA and TCR sequencing of the proliferated recipient T cells. Subsequently, these TCR clones were traced in the TRM cells of kidney explants, which were also subjected to single-cell RNA and TCR sequencing. The proportion of TRM cells expressing an alloreactive TCR in the four kidney explants varied from 0% to 9%. Notably, these alloreactive TCRs were predominantly found among CD4+ and CD8+ TRM cells with an effector phenotype. Intriguingly, alloreactive clones were present not only in recipient-derived TRM cells but also in donor-derived TRM cells, constituting up to 4% of the donor population, suggesting the presence of self-reactive TRM cells. Overall, our study demonstrates that T cells with alloreactive potential present in the peripheral blood prior to transplantation can infiltrate the kidney transplant and adopt a TRM phenotype.

2024-03-01 | GSE249197 | GEO

GVHD-mediated Vicious Cascade: Impaired Reconstitution of Immunosuppressive Donor Plasmacytoid Dendritic Cells

Project description:In patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT), severe graft-versus-host disease (GVHD) is tied to failed donor plasmacytoid DC (pDC) reconstitution. The mechanism whereby GVHD causes donor pDC defects and the precise role donor pDCs play in GVHD remain poorly understood. pDCs develop from HSCs in successive stages through Flt3 signaling-dependent differentiation, beginning as multi-potent progenitors (MPPs) and later becoming common DC progenitors. We observed that MPPs were critical for sustaining pDCs and were severely depleted during GVHD. Loss of MPPs was associated with decreased amounts of MPP-producing HSCs and mTOR activation-induced cell death of proliferating MPPs. Additionally, GM-CSF derived from alloreactive T cells subverted MPP production of pDCs. Together, GVHD and alloreactive T cells caused donor pDC defects by impairing the generation, maintenance and differentiation of HSCs and MPPs. Importantly, pDCs suppressed the proliferation and expansion of activated autologous CD4+ T cells via a type I-IFN signaling-dependent mechanism. Transfer of donor pDCs early after transplantation repressed GVHD and preserved potent GVL effects, significantly improving the survival of leukemia mice undergoing allo-HSCT. Our findings identify novel strategies that improve the recovery of donor pDCs early after allo-HSCT and thus may represent an effective therapy to control GVHD. Our findings have broad implications for other diseases in which functional DC development is impaired, such as chronic infections, autoimmunity and cancer.

2021-01-06 | GSE143788 | 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.

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