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BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

ABSTRACT: BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

PROVIDER: PRJNA498403 | ENA |

REPOSITORIES: ENA

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BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

Project description:CD4+ T helper 17 (Th17) cells protect vertebrate hosts from extracellular pathogens at mucosal surfaces. Th17 cells form from naïve precursors when signals from the T cell antigen receptor (TCR) and certain cytokine receptors induce the expression of the RORγt transcription factor, which activates a set of Th17-specific genes. Using T cell-specific loss-of-function experiments we find that two components of the Polycomb Repressive Complex 1.1 (PRC1.1), BCL6 corepressor (BCOR) and KDM2B, which helps target the complex to unmethylated CpG DNA islands, are required for optimal Th17 cell formation in mice after Streptococcus pyogenes infection. Genome-wide expression and BCOR chromatin immunoprecipitation studies revealed that BCOR directly represses Lef1, Runx2, and Dusp4, whose products inhibit Th17 differentiation. Together, the results suggest that PRC1.1 components, BCOR and KDM2B, work together to enhance Th17 cell formation by repressing Th17 fate suppressors.

2019-04-26 | GSE121766 | GEO

BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors.

Project description: Not available

| S-EPMC6547868 | biostudies-literature

BCL6 corepressor regulates androgen signaling and viability of prostate cancer cells

Project description:To analyze the role of BCOR (BCL6 corepressor) in androgen signaling, we used ChIP-seq to analyze chromatin binding of BCOR and positioning of H2AK119ub histone mark in androgen and vehicle treated VCaP cells. The role of BCOR in transcription regulation and positioning of H2AK119ub histone mark was analyzed from BCOR depleted (siBCOR) and control (siNON) treated VCaP cells in andorgen and vehicle treatments.

2019-12-31 | GSE122572 | GEO

Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation

Project description:Ectopic lymphoid tissue containing B cells forms in the meninges at late stages of human multiple sclerosis (MS) and when neuroinflammation is induced by interleukin (IL)-17 producing T helper (Th17) cells in rodents. B cell differentiation and the subsequent release of class-switched immunoglobulins have been speculated to occur in the meninges, but the exact cellular composition and underlying mechanisms of meningeal-dominated inflammation remain unknown. Here, we performed in depth characterization of meningeal vs. parenchymal Th17-induced rodent neuroinflammation. The most pronounced cellular and transcriptional differences between these compartments was the localization of B cells exhibiting a follicular phenotype exclusively to the meninges. Correspondingly, meningeal but not parenchymal Th17 cells, acquired a B cell-supporting phenotype and resided in close contact with B cells. This preferential B cell tropism for the meninges and the formation of meningeal ectopic lymphoid tissue was partially dependent on the expression of the transcription factor Bcl6 in Th17 cells, that is required in other T cell lineages to induce isotype class-switching in B cells. A function of Bcl6 in Th17 cells was only detected in vivo and was reflected by the induction of B cell-supporting cytokines, the appearance of follicular B cells in the meninges, and of immunoglobulin class-switching in the CSF. We, thus, identify the induction of a B cell-supporting meningeal microenvironment by Bcl6 in Th17 cells as a novel mechanism controlling compartment-specificity in neuroinflammation.

2021-07-30 | GSE178085 | GEO

BCL6 corepressor regulates androgen signaling and viability of prostate cancer cells

Project description:BCL6 corepressor regulates androgen signaling and viability of prostate cancer cells

| PRJNA505654 | ENA

Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation

Project description:Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation

| PRJNA737340 | ENA

RNA-seq analysis of the effects of BCL6-inhibiting and BCL6-degrading compounds in lymphoma cell lines

Project description:The goal of this experiment is to measure the changes in gene expression induced by small molecules that either inhibit the interaction of the transcription factor BCL6 with co-repressor proteins, or that induce degradation of BCL6, in lymphoma cell lines.

2017-09-17 | GSE94099 | GEO

Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

Project description:Innate lymphoid cells (ILC) are similar to T helper (Th) cells in expression of cytokines and transcription factors. For example, RORγt is the lineage-specific transcription factor for both ILC3 and Th17 cells. However, the ILC counterpart for BCL6-expressing T follicular helper (Tfh) cells has not been defined. Here, we report that in the ILC compartment, BCL6 is selectively co-expressed with not only CXCR5, but also RORγt and CCR6 in ILC3 from multiple tissues. BCL6-deficient ILC3 produce enhanced levels of IL-17A and IL-22. More importantly, phenotypic and single-cell ATAC-seq analysis show that absence of BCL6 in mature ILC3 increases the numbers of ILC1 and transitional cells co-expressing ILC3 and ILC1 marker genes. A lineage-tracing experiment further reveals BCL6+ ILC3 to ILC1 trans-differentiation under steady state. Lastly, microbiota promote BCL6 expression in colonic CCR6+ ILC3, and thus reinforce their stability. Collectively, our data have demonstrated that CCR6+ ILC3 have both Th17 and Tfh programs and that BCL6 expression in these cells functions to maintain their lineage identity.

2022-12-27 | GSE221341 | GEO

Cyclic AMP-responsive element-binding protein (CREB) is critical in autoimmunity by promoting Th17 but inhibiting Treg differentiation

Project description:The molecular mechanisms that govern differential T cell development into pro-inflammatory Th17 vs. regulatory T (Treg) cells remain unclear. Here, we show that selective deletion of CREB in T cells or Th17 cells impaired Th17 differentiation in vitro and in vivo, and led to resistance to autoimmune diseases. Mechanistically, CREB, activated by CD3-PKC-ϴ signaling, plays a key role in regulating Th17 differentiation, at least in part through directly binding to the Il17-Il17f gene locus. Unexpectedly, although dispensable for FOXP3 expression and for the homeostasis and function of thymus-derived Treg cells, CREB negatively regulates the survival of TGF-β-induced Treg cells, and deletion of CREB resulted in increased FOXP3+ Treg cells in the intestine and protection in a colitis model. Thus, CREB is critical in autoimmune diseases by promoting Th17 and inhibiting de novo Treg generation.

2016-04-19 | GSE80375 | GEO