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Population RNA-seq from Th17 cells differentiated in vitro under pathogenic (Th17p) and non-pathogenic (Th17n) conditions with DHEA or EGCG

ABSTRACT: We investigated the effect of glycolytic inhibitors on Th17 differentiation

ORGANISM(S): Mus musculus

PROVIDER: GSE290297 | GEO | 2025/05/14

REPOSITORIES: GEO

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Population RNA-seq from Th17 cells differentiated in vitro under pathogenic (Th17p) and non-pathogenic (Th17n) conditions with DHEA or EGCG

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Population transcriptional profiling of KO or WT cells,, differentiated in vitro for 48-96h towards Th17 cells

Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Population transcriptional profiling of KO or WT cells,, differentiated in vitro for 48-96h towards Th17 cells

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Project description:It is well known that some pathogenic cells have enhanced glycolysis, the regulatory network leading to increased glycolysis are not well characterized. Here, we show that CNS-infiltrated pathogenic TH17 cells from diseased mice specifically upregulate glycolytic pathway genes compared to homeostatic intestinal TH17 cells. Bioenergetic assay and metabolomics analyses indicate that in vitro derived pathogenic TH17 cells are highly glycolytic compared to nonpathogenic TH17 cells. Chromatin landscape analyses demonstrate TH17 cells in vivo show distinct chromatin states, and pathogenic TH17 cells show enhanced chromatin accessibility at glycolytic genes with NF-kB binding sites. Mechanistic studies reveal that miR-21 targets the E3 ubiquitin ligase Peli1-c-Rel pathway to promote glucose metabolism of pathogenic TH17 cells. Therapeutic targeting c-Rel-mediated glycolysis in pathogenic TH17 cells represses autoimmune diseases. These findings extend our understanding of the regulation TH17 cell glycolysis in vivo and provide insights for future therapeutic intervention to TH17 cell mediated autoimmune diseases.

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Population transcriptional profiling of KO or WT cells,, differentiated in vitro for 48-96h towards Th17 cells

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Expression data from in vitro versus in vivo differentiated Th17 cells

Project description:In vitro differentiated Th17 have a distinct expression profile compared to in vivo differentiated Th17 Several conditions of Th17 cells were tested, with 2-3 replicates per condition.

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Project description:In vitro differentiated Th17 have a distinct expression profile compared to in vivo differentiated Th17

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