Prostaglandin and prostacyclin regulation of Th1 responses [ptgir_ptgis_sirna]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1220136 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR32258311.fastq.gz | Fastqsanger.gz | |||
| SRR32258318.fastq.gz | Fastqsanger.gz | |||
| SRR32258321.fastq.gz | Fastqsanger.gz | |||
| SRR32258327.fastq.gz | Fastqsanger.gz |
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Project description:Prostaglandin and prostacyclin regulation of Th1 responses [ptgir_ko]
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Project description:The progressive decline of CD8 T cell effector function, also known as T cell “exhaustion” (Tex), is a major contributor to immune evasion in cancer, yet the molecular mechanisms that promote this decline remain poorly understood. Here, we identify the prostaglandin I2 receptor (PTGIR) as a cell-intrinsic driver of CD8 T cell dysfunction. Transcriptional profiling of dysfunctional CD8 T cells from chronic infection and cancer reveals enrichment of the Kelch-like ECH-associated protein 1 (KEAP1)-Nuclear factor erythroid 2-related factor 2 (NRF2) signaling axis, which mediates cellular adaptations to oxidative stress, in terminally exhausted (Tex-term) CD8 T cells. Increasing NRF2 activity in CD8 T cells (via conditional deletion of KEAP1) promotes increased glutathione production and antioxidant defense yet accelerates the development of terminally exhausted (PD-1+/TIM-3+) CD8 Tex cells in response to chronic infection or tumor challenge. NRF2 promotes the increased expression of PTGIR, a receptor for the circulating eicosanoid prostacyclin, in CD8 T cells. Silencing PTGIR expression restores the anti-tumor function of KEAP1-deficient CD8 T cells. Moreover, lowering PTGIR expression in CD8 T cells both reduces terminal exhaustion and enhances T cell effector responses (i.e. IFN-gamma and granzyme production) to chronic infection and cancer. Mechanistically, PTGIR signaling blunts both bioenergetic metabolism and effector cytokine production in CD8 T cells and promotes a Tex cell signature marked by high expression of interferon-stimulated genes (ISGs). Together, these results identify the prostacyclin receptor PTGIR as an NRF2-regulated immune checkpoint that regulates CD8 T cell fate decisions between effector and exhausted states.
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