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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

ABSTRACT: IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

PROVIDER: PRJNA667100 | ENA |

REPOSITORIES: ENA

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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

Project description:IL-27 is an immunoregulatory cytokine that suppresses inflammation through multiple mechanisms including induction of IL-10, but the transcriptional network mediating its diverse functions remains unclear. Combining temporal RNA profiling with computational algorithms, we predict 79 transcription factors induced by IL-27 in T cells. We validate 11 known and discover 5 positive (Cebpb, Fosl2, Tbx21, Hlx, Atf3) and 2 negative (Irf9, Irf8) Il10 regulators, generating an experimentally refined regulatory network for Il10. We report two central regulators Prdm1 and Maf that cooperatively drive the expression of signature genes induced by IL-27 in Type 1 regulatory T cells, mediate IL-10 expression in all T helper cells, and determine the regulatory phenotype of colonic Foxp3+regulatory T cells. Prdm1/Maf double-knockout mice develop spontaneous colitis, phenocopying the ll10 deficient mice. Our work provides insights for IL-27 driven transcriptional networks and identifies two shared Il10 regulators that orchestrate immunoregulatory programs across T helper cell subsets.

2020-12-21 | GSE158967 | GEO

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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO Tr1 ATAC-seq]

Project description:IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO Tr1 ATAC-seq]

| PRJNA666212 | ENA

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Project description:Prdm1

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Transcriptional profiling of human IL-9R+ T helper cells in presence of recombinant IL-9 against untreated control

Project description:To study the effect of paracrine interleukin-9 (IL-9) on T helper cells, we incubated IL-9R+ T helper cells isolated from blood (5 samples) and skin (3 samples) with or without IL-9 for 12h and the transcriptome was analyzed by bulk RNA-seq.

2022-10-31 | E-MTAB-12204 | biostudies-arrayexpress

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq05, bulk-RNAseq)

Project description:We have shown that TGFb in combination with IL-6 potently induces a T follicular helper cell (Tfh) cell phenotype in activated murine CD4+ T cells in vitro. The transcription factor c-Maf critically contributes to the differentiation of Tfh cells in vitro and in vivo.

2024-03-01 | GSE243257 | GEO

RNAseq of Wild Type and Prdm1/c-Maf cDKO CD8+ Tumor infiltrating lymphocytes isolated from B16F10 melanoma

Project description:Expression of co-inhibitory receptors, such as CTLA-4 and PD-1, on effector T cells is a key mechanism for ensuring immune homeostasis. Dysregulated co-inhibitory receptor expression on CD4+ T cells promotes autoimmunity while sustained overexpression on CD8+ T cells promotes T cell dysfunction or exhaustion, leading to impaired ability to clear chronic viral infections and cancer. Here, we used RNA and protein expression profiling at single-cell resolution to identify a module of co-inhibitory receptors that includes not only several known co-inhibitory receptors (PD-1, Tim-3, Lag-3, and TIGIT), but also a number of novel surface receptors. We functionally validated two novel co-inhibitory receptors, Activated protein C receptor (Procr) and Podoplanin (Pdpn). The module of co-inhibitory receptors is co-expressed in both CD4+ and CD8+ T cells and is part of a larger co-inhibitory gene program that is shared by non-responsive T cells in multiple physiological contexts and is driven by the immunoregulatory cytokine IL-27. Computational analysis identified the transcription factors Prdm1 and c-Maf as cooperative regulators of the co-inhibitory module, which we validated experimentally. This molecular circuit underlies the co-expression of co-inhibitory receptors in T cells and identifies novel regulators of T cell function with the potential to regulate autoimmunity and tumor immunity.

2018-06-14 | GSE113221 | GEO

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