Hspa8 and ICAM-1 identified as damage-induced mediators of gd T cell activation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA713337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13927611.fastq.gz | Fastqsanger.gz | |||
| SRR13927612.fastq.gz | Fastqsanger.gz | |||
| SRR13927613.fastq.gz | Fastqsanger.gz | |||
| SRR13927614.fastq.gz | Fastqsanger.gz | |||
| SRR13927615.fastq.gz | Fastqsanger.gz |
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Project description:IL-17-producing gd T (Tgd17) cells are early mediators of immunity and autoimmunity that undergo effector programming in the thymus. While Vg subset-restricted regulators of Tgd17 specialization are known, a universal type 17 commitment factor for all gd T cells remains undefined. In this study, we identify the transcription factor c-Maf as an essential and uniform regulator of Tgd17 differentiation and maintenance. The absolute lineage block caused by Maf deficiency reveals a critical effector acquisition checkpoint at the immature CD24+ CD45RBlo gd thymocyte stage. Here, c-Maf enforces Tgd17 identity by promoting chromatin accessibility and activating expression of lineage-defining RORgt and key type 17 program genes, while coordinately antagonizing the negative regulator TCF1, which promotes the alternative IFNg+ Tgd1 fate. During specialization, c-Maf expression is tuned by gdTCR signal strength, implicating c-Maf as a rheostat controlling effector gd T cell generation and connecting gdTCR signals to a core node in the Tgd17 network.
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