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Differential Metabolic Requirement Governed by Transcription Factor c-Maf Dictates Innate γδT17 Effector Functionality in Mice and Humans

ABSTRACT: Differential Metabolic Requirement Governed by Transcription Factor c-Maf Dictates Innate γδT17 Effector Functionality in Mice and Humans

PROVIDER: PRJNA797668 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17631854_1.fastq.gz	Fastqsanger.gz
	SRR17631854_2.fastq.gz	Fastqsanger.gz
	SRR17631855_1.fastq.gz	Fastqsanger.gz
	SRR17631855_2.fastq.gz	Fastqsanger.gz
	SRR17631856_1.fastq.gz	Fastqsanger.gz

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Differential Metabolic Requirement Governed by Transcription Factor c-Maf Dictates Innate γδT17 Effector Functionality in Mice and Humans

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Differential metabolic requirement governed by transcription factor c-Maf dictates innate γδT17 effector functionality in mice and humans.

Project description:Cellular metabolism has been proposed to govern distinct γδ T cell effector functions, but the underlying molecular mechanisms remain unclear. We show that interleukin-17 (IL-17)-producing γδ T (γδT17) and interferon-γ (IFN-γ)-producing γδ T (γδT1) cells have differential metabolic requirements and that the rate-limiting enzyme isocitrate dehydrogenase 2 (IDH2) acts as a metabolic checkpoint for their effector functions. Intriguingly, the transcription factor c-Maf regulates γδT17 effector function through direct regulation of IDH2 promoter activity. Moreover, mTORC2 affects the expression of c-Maf and IDH2 and subsequent IL-17 production in γδ T cells. Deletion of c-Maf in γδ T cells reduces metastatic lung cancer development, suggesting c-Maf as a potential target for cancer immune therapy. We show that c-Maf also controls IL-17 production in human γδ T cells from peripheral blood and in oral cancers. These results demonstrate a critical role of the transcription factor c-Maf in regulating γδT17 effector function through IDH2-mediated metabolic reprogramming.

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