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

PROVIDER: PRJNA957431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24219100_1.fastq.gz	Fastqsanger.gz
	SRR24219100_2.fastq.gz	Fastqsanger.gz
	SRR24219101_1.fastq.gz	Fastqsanger.gz
	SRR24219101_2.fastq.gz	Fastqsanger.gz
	SRR24219102_1.fastq.gz	Fastqsanger.gz

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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]

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.

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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

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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]

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

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

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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.

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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.

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Expression Profile of alloreactive CD8 and CD4 induced regulatory T cells

Project description:Adoptive natural regulatory T cell (nTreg) therapy has improved the outcome for patients suffering from graft-versus-host disease (GVHD) following allogeneic hematopoietic cell transplantation (allo-HCT). However, fear of broad immune suppression and subsequent dampening of beneficial graft-versus-leukemic (GVL) responses remains a challenge. To address this concern, we generated alloreactive induced Tregs (iTregs) from resting CD4 or CD8 T cells and tested their ability to suppress GVH and maintain GVL responses. We utilized major mismatched and haploidentical murine models of HCT with host-derived lymphoma or leukemia cell lines to evaluate GVH and GVL responses simultaneously. Alloreactive CD4 iTregs were effective in preventing GVHD, but abrogated the GVL effect against aggressive leukemia. Alloreactive CD8 iTregs moderately attenuated GVHD while sparing the GVL effect. Hence, we reasoned that using a combination of CD4 and CD8 iTregs could achieve the optimal goal of allo-HCT. Indeed, the combinational therapy was superior to CD4 or CD8 iTreg singular therapy in GVHD control; importantly, the combinational therapy maintained GVL responses. Cellular analysis uncovered potent suppression of both CD4 and CD8 effector T cells by the combinational therapy that resulted in effective prevention of GVHD, which could not be achieved by either singular therapy. Gene expression profiles revealed alloreactive CD8 iTregs possess elevated expression of multiple cytolytic molecules compared to CD4 iTregs, which likely contributes to GVL preservation. Our study uncovers unique differences between alloreactive CD4 and CD8 iTregs that can be harnessed to create an optimal iTreg therapy for GVHD prevention with maintained GVL responses.

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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.

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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.

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