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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE230286 | 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 [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 [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 [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

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

Adenosine Selectively Depletes Alloreactive T Cells to Prevent GVHD While Conserving Immunity to Viruses and Leukemia.

Project description:Selective depletion (SD) of alloreactive T cells from allogeneic hematopoeitic stem cell transplants to prevent graft-versus-host disease (GVHD) without compromising immune reconstitution and antitumor responses remains a challenge. Here, we demonstrate a novel SD strategy whereby alloreacting T cells are efficiently deleted ex vivo with adenosine. SD was achieved in human leukocyte antigen (HLA) mismatched cocultures by multiple exposures to 2 mmol/l adenosine over 7 days. Adenosine depleted greater than to 90% of alloproliferating T cells in mismatched, haploidentical, and matched sibling pairs while conserving response to third-party antigens. Alloreactive CD4 and CD8 T cells were targeted for depletion while NK and B cells were preserved. Our novel approach also preserved nonalloreactive naive, central, and effector memory T-cell subsets, Tregs, and notably preserved T-cell responses against DNA viruses that contribute to transplant related mortality after allogeneic hematopoeitic stem cell transplants. Additionally, T cells recognizing leukemia-associated antigens were efficiently generated in vitro from the cell product post-SD. This study is the first to demonstrate that adenosine depletion of alloactivated T cells maintains a complete immune cell profile and recall viral responses. Expansion of tumor antigen-specific subsets postdepletion opens the possibility of generating T-cell products capable of graft-versus-tumor responses without causing GVHD.

| S-EPMC5113112 | biostudies-literature

IFNγR signaling mediates alloreactive T-cell trafficking and GVHD.

Project description:The clinical goal of allogeneic hematopoietic stem cell transplantation (allo-HSCT) is to minimize GVHD while maintaining GvL. Here, we show that interferon γ receptor-deficient (IFNγR(-/-)) allogeneic Tconv, which possess normal alloreactivity and cytotoxicity, induce significantly less GVHD than wild-type (WT) Tconv. This effect is mediated by altered trafficking of IFNγR(-/-) Tconv to GVHD target organs, especially the gastrointestinal (GI) tract. We show that the chemokine receptor CXCR3 is induced via IFNγR-mediated signaling and partially contributes to the trafficking of WT Tconv to GVHD target organs. Indeed, CXCR3(-/-) Tconv recapitulate the reduced GVHD potential of IFNγR(-/-) Tconv in a minor-mismatched GVHD model. Most importantly, IFNγR(-/-) (and CXCR3(-/-)) Tconv mediate a robust and beneficial GvL effect. In addition, we show that IFNγR(-/-) regulatory T cells (Tregs) are fully suppressive in vitro although defective in suppressor function in vivo and that WT Tregs suppress GVHD in vivo only when allogeneic Tconv produce interferon γ (IFNγ), suggesting that the IFNγR signaling pathway is the major mechanism for both Tregs and Tconv to migrate to GVHD target organs. Finally, pharmacologic inhibition of IFNγR signaling with inhibitors of JAK1/JAK2, which are mediators of IFNγR signaling, results in the decreased expression of CXCR3 and reduced GVHD and improved survival after allo-HSCT and this effect is mediated by altered trafficking of Tconv to GVHD target organs.

| S-EPMC3496960 | biostudies-literature

PKCtheta is required for alloreactivity and GVHD but not for immune responses toward leukemia and infection in mice.

Project description:When used as therapy for hematopoietic malignancies, allogeneic BM transplantation (BMT) relies on the graft-versus-leukemia (GVL) effect to eradicate residual tumor cells through immunologic mechanisms. However, graft-versus-host disease (GVHD), which is initiated by alloreactive donor T cells that recognize mismatched major and/or minor histocompatibility antigens and cause severe damage to hematopoietic and epithelial tissues, is a potentially lethal complication of allogeneic BMT. To enhance the therapeutic potential of BMT, we sought to find therapeutic targets that could inhibit GVHD while preserving GVL and immune responses to infectious agents. We show here that T cell responses triggered in mice by either Listeria monocytogenes or administration of antigen and adjuvant were relatively well preserved in the absence of PKC isoform theta (PKCtheta), a key regulator of TCR signaling. In contrast, PKCtheta was required for alloreactivity and GVHD induction. Furthermore, absence of PKCtheta raised the threshold for T cell activation, which selectively affected alloresponses. Most importantly, PKCtheta-deficient T cells retained the ability to respond to virus infection and to induce GVL effect after BMT. These findings suggest PKCtheta is a potentially unique therapeutic target required for GVHD induction but not for GVL or protective responses to infectious agents.

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