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TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq01, bulk-RNAseq)

ABSTRACT: TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq01, bulk-RNAseq)

PROVIDER: PRJNA814700 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18293039.fastq.gz	Fastqsanger.gz
	SRR18293040.fastq.gz	Fastqsanger.gz
	SRR18293041.fastq.gz	Fastqsanger.gz
	SRR18293042.fastq.gz	Fastqsanger.gz
	SRR18293043.fastq.gz	Fastqsanger.gz

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

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

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TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

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TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq03, bulk-RNAseq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq03, bulk-RNAseq)

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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.

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TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

Project description:Naive murine CD4+ T cells from GREAT/SMART-17A mice were cultured under Th1 or Tfh(1 ng/ml TGF-β)-polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days; sorted by flow cytometry on IFNg+ (Th1), or CXCR5-IL17A+ (Th17) and CXCR5+IL17A- (Tfh); and subjected to bulk RNA-seq.

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Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

Project description:Genome-wide analysis of Jarid2, Suz12, and c-Maf binding and H3K27me3 profiling in miR-155 KO and WT Th17 performed by ChIP-seq. We found that Jarid2 and c-Maf is differentially expressed in absence of miR-155 and they compete for binding to the Il22 promoter. We highlight targets of Jarid2 and Suz12 in miR-155 KO Th17 cells that are epigenetically silenced by increased H3K27me3 status. Furthermore, genome-wide analysis through Suz12 ChIP-exo in WT and Jarid2fl/fl;CD4cre Th17 reveals defects in PRC2 recruitment in abscence of Jarid2 that results in derepression of genes in Th17 cells. Thus, one main function of miR-155 is to curb epigenetic silencing by targeting Jarid2. Examination of Jarid2, Suz12, c-Maf binding and H3K27me3 changes in miR-155 KO and WT Th17.

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Germinal Center T follicular helper (GC-Tfh) cell impairment in chronic HIV infection involves c-Maf signaling [microarray]

Project description:We have recently demonstrated that the function of T follicular helper (Tfh) cells obtained from lymph nodes (LN) of HIV-infected individuals is impaired. We found that these cells were unable to provide proper help to germinal center (GC)-B cells, as observed by altered and inefficient anti-HIV antibody response and premature death of memory B cells. The underlying molecular mechanisms of this dysfunction remain poorly defined. Herein, we have used a unique transcriptional approach to identify these molecular defects. We consequently determined the transcriptional profiles of LN GC-Tfh cells following their interactions with LN GC-B cells from HIV-infected and HIV-uninfected individuals, rather than analyzing resting ex-vivo GC-Tfh cells. We observed that proliferating HIV-infected GC-Tfh cells were transcriptionally different than those from HIV-uninfected individuals, displaying a significant downregulation of immune- and GC-Tfh-associated pathways and genes compared to cells from uninfected individuals. Our results strongly demonstrated that MAF (coding for the transcription factor c-Maf) and its upstream signaling pathway mediators (IL6R and STAT3) were significantly downregulated in HIV-infected subjects, which could contribute to the impaired GC-Tfh and GC-B cell functions reported during infection. We further showed that c-Maf function was associated with the adenosine pathway and that the signaling upstream c-Maf could be partially restored by adenosine deaminase -1 (ADA-1) supplementation. Overall, we identified a novel mechanism that contributes to GC-Tfh impairment during HIV infection. Understanding how GC-Tfh function is altered in HIV is crucial and could provide critical information about the mechanisms leading to the development and maintenance of effective anti-HIV antibodies.

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Germinal Center T follicular helper (GC-Tfh) cell impairment in chronic HIV infection involves c-Maf signaling [RNA-seq]

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Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

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