Prostaglandin and prostacyclin regulation of Th1 responses [ptgir_ko]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1220022 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32255100.fastq.gz | Fastqsanger.gz | |||
| SRR32255101.fastq.gz | Fastqsanger.gz | |||
| SRR32255102.fastq.gz | Fastqsanger.gz | |||
| SRR32255103.fastq.gz | Fastqsanger.gz | |||
| SRR32255104.fastq.gz | Fastqsanger.gz |
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Project description:Prostaglandin and prostacyclin regulation of Th1 responses [ptgir_ptgis_sirna]
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Project description:Metabolic reprogramming is an integral component of normal Th1 induction and contraction. Whereas Th1 inducing signals are largely defined, the pathways underlying timely Th1 contraction remain poorly understood. Here, we show that a CD4+ T cell-intrinsic prostanoid lipid mediator production and signaling machinery, controlled by cell-autonomous complement C5, governs the Th1 shutdown program.
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2022-12-16 | E-MTAB-12437 | biostudies-arrayexpress
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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Project description:Effect of prostacyclin in ovarian carcinoma
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Project description:Induction of long-lived antibody responses during infection or vaccination is often essential for subsequent protection, but the relative contributions of T follicular helper (Tfh) cells and T helper 1 (Th1) cells for induction of antigen specific antibody responses to viruses are unclear. Here, we establish an acute Zika virus (ZIKV) infection model in immunocompetent mice, and show that ZIKV infection elicits robust Th1-like Tfh cell and protective antibody responses. While these Th1-like Tfh cells share phenotypic and transcriptomic profiles with both Tfh and Th1 cells, they also have unique surface markers and gene expression characteristics, and are dependent on T-bet for their development. Th1-like Tfh cells, but not Th1 cells, are essential for class switching of ZIKV-specific IgG2c antibodies and maintenance of long-term neutralizing antibody responses. Our study suggests that specific modulation of the Th1-like Tfh cell response during infection or vaccination may augment the induction of antiviral antibody response to ZIKV and other viruses.
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