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Assessement of transcriptional consequences of CD27 signaling on Tregs during Th17 polarization

ABSTRACT: Assessement of transcriptional consequences of CD27 signaling on Tregs during Th17 polarization

PROVIDER: PRJNA498509 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8110710_1.fastq.gz	Fastqsanger.gz
	SRR8110710_2.fastq.gz	Fastqsanger.gz
	SRR8110711_1.fastq.gz	Fastqsanger.gz
	SRR8110711_2.fastq.gz	Fastqsanger.gz
	SRR8110712_1.fastq.gz	Fastqsanger.gz

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Assessement of transcriptional consequences of CD27 signaling on Tregs during Th17 polarization

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Project description:IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. Gene array analysis on Stat6 and T-bet double deficient Th17 cells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TGFbeta, and associated with Th17 IL-10 production. Both c-Maf and IL-10 induction during Th17 polarization depended on Stat3, but not Stat6 or Stat1, and mechanistically differed from IL-10 regulation by Th2 or IL-27 signals. TGFbeta was also synergistic with IL-27 to induce c-Maf, and induced Stat1 independent IL-10 expression in contrast to IL-27 alone. Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6 deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression through binding to a MARE motif in the IL-10 promoter. Together, these data reveal a novel role for c-Maf in regulating T effector development, and suggest that TGFbeta may antagonize Th17 immunity by IL-10 production through c-Maf induction. Our recent studies showed that IL-6 combined with TGFbeta differed from IL-6 combined with IL-23 for IL-10 production and pathogenic activities in CD4 T cells deficient in Stat6 and T-bet, despite similar IL-17 production. We performed gene array analysis on Stat6 and T-bet double deficient cells. We rationalized that by comparing gene expression in cells treated with IL-6 plus TGFbeta versus TGFbeta alone, we would be able to identify genes specific for standard Th17 polarization, and responsible for both IL-17 and IL-10 expression. By next comparing gene expression in cells treated with IL-6 plus TGFbeta versus IL-6 plus IL-23, we could eliminate molecules involved solely in IL-17 regulation, and obtain genes specifically responsible for IL-10 regulation.

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