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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

ABSTRACT: Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

PROVIDER: PRJNA922456 | ENA |

REPOSITORIES: ENA

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

Project description:Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [RNA-Seq]

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of myeloid and lymphoid cell type diversity with our m-RNA sequencing interrogation.

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas [scRNA-seq]

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Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

Project description:The brain tumor immune microenvironment (TIME) continuously evolves during glioma progression, but only a limited view of a highly complex glioma associated immune contexture across isocitrate dehydrogenase mutation (IDH) classified gliomas is known. Herein, we present an unprecedentedly comprehensive view of T cells from brain TIME at single cell resolution, which served as part of our pan-cancer T cell atlas analysis.

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Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

Project description:Gene expression profile of T cells from Isocitrate Dehydrogenase (IDH) stratified human gliomas at single cell level

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Loss of retinoic acid signaling drives immune escape in IDH mutant gliomas

Project description:Gliomas are immunologically cold tumors that can be broken into several categories based on either RNA expression profiles or methylation profiles, with isocitrate dehydrogenase (IDH) mutations defining a major segregration between types. IDH mutant gliomas often exhibit defects in the retinoic acid pathway. We treated mice harboring IDH mutant gliomas with all-trans retinoic acid, and found that this treatment cause reductions in tumor growth and a swith in immune profiles in the tumor microenvironment.

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Immune landscape of Isocitrate Dehydrogenase (IDH) stratified human gliomas

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

2023-06-05 | GSE222522 | GEO

Tryptophan metabolism drives dynamic immunosuppressive myeloid states in IDH-mutant gliomas [CEL-Seq2]

Project description:Intratumoral microglia and MΦ constitute up to 70% of the tumor mass of high-grade gliomas (HGG) with profound impact on hallmarks of malignancy such as angiogenesis and immunosuppression. The dynamics and functional states of intratumoral myeloid cells during tumor progression and the molecular mechanisms controlling them are poorly understood. Here we define homeostatic and antigen-presenting myeloid cellular states in experimental and human HGG by longitudinal single-cell RNA-sequencing and combined transcriptome and proteome profiling, respectively. During glioma progression, myeloid cells gradually shift from a homeostatic to a tumor-associated effector state. We show that these dynamics are under strict control by early changes in resident microglia and the tumor genotype: In gliomas with mutations in isocitrate dehydrogenase (IDH), a disease-defining driver mutation, differentiation of invaded myeloid cells was blocked resulting in an immature, immunosuppressive phenotype. In late-stage IDH-mutant gliomas, monocyte-derived MΦ drive a tolerogenic remodeling of the glioma microenvironment thus preventing T-cell response. We define the molecular mechanism responsible for blocking functional differentiation in IDH-mutant gliomas to be causally related to enhanced metabolization of tryptophan to kynurenine, an endogenous ligand of the aryl hydrocarbon receptor (AHR), leading to a time-dependent uptake of extracellular tryptophan via LAT1-CD98 by intratumoral myeloid cells. Consequently, the immunosuppressive phenotype in IDH-mutant glioma models was reversed by pharmacologic inhibition of LAT1-CD98 or AHR. Thus, we provide evidence for a tumor genotype-dependent dynamic network of resident and recruited intratumoral myeloid cells shaping the immune microenvironment of IDH-mutant HGG and identify tryptophan metabolism as a viable therapeutic target for the immunotherapy of IDH-mutant tumors.

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