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Quantitative Transcriptome Analysis of RIPK1-KO CD4 T cells

ABSTRACT: Quantitative Transcriptome Analysis of RIPK1-KO CD4 T cells

PROVIDER: PRJNA809404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18101441.fastq.gz	Fastqsanger.gz
	SRR18101442.fastq.gz	Fastqsanger.gz
	SRR18101443.fastq.gz	Fastqsanger.gz
	SRR18101444.fastq.gz	Fastqsanger.gz

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Quantitative Transcriptome Analysis of RIPK1-KO CD4 T cells

Project description:RIPK1 is a key signaling molecule controlling cell death and inflammation through both scaffold and kinase functions of RIPK1. Human RIPK1 deficiency causes immunodeficiency and inflammatory diseases. Here we analyzed the functional roles of RIPK1 in CD4 T cells.

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RIPK1 phosphorylation in INPP5D KO cells

Project description:We identified and quantified RIPK1 phosphorylation sites in INPP5D KO cells and find Y383 phosphorylation was increased in INPP5D cells compared to control cells. Next, we found that Y383 phosphorylation enhance binding of INPP5D with RIPK1 to inhibit RIPK1 activation.

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Project description:The T cell population size is stringently controlled before, during, and after immune responses, as improper cell death regulation can result in autoimmunity and immunodeficiency. RIPK1 is an important regulator of peripheral T cell survival and homeostasis. However, whether different peripheral T cell subsets show a differential requirement for RIPK1 and which programmed cell death pathway they engage in vivo remains unclear. In this study, we used mesenteric lymph node (mLN) cells of Ripk1 KO mice, Ripk1/Casp8 double KO mice and their respective wild types to investigate this.

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Next Generation Sequencing to check the enrichment of RIPK1/BAF on chromatin, RIPK1-dependent chromatin state and RIPK1-dependent transcriptome during inflammatory responses.

Project description:RIPK1 is a master regulator of multiple cell death pathways, including apoptosis and necroptosis, and inflammation. Multiple RIPK1 inhibitors have been advanced into human clinical trials as new therapeutics for human inflammatory and neurodegenerative diseases, including ALS and AD. However, while the mechanism of cytosolic RIPK1 in control of cell death has been extensively investigated, how the activation of RIPK1 may promote transcription of proinflammatory cytokines is unclear as a nuclear function of RIPK1 has not been explored, nor is it clear if and how RIPK1 kinase activity may directly mediate inflammation independent of cell death. Here we show that nuclear RIPK1 is recruited by specific transcription factors and binds to the BAF complex on active enhancers and promoters marked by H3K4me1 and H3K27ac. Nuclear RIPK1 mediates the phosphorylation of SMARCC2, a key component of the BAF complex, to promote chromatin remodeling and the transcription of specific proinflammatory genes. Our results suggest that RIPK1 kinase serves a transcriptional coregulator in nucleus that can transmit extracellular stimuli to BAF complex to modulate the chromatin accessibility and directly regulate the transcription of specific genes involved in mediating inflammatory responses.

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T cell-specific RIPK1 ablation results in villus atrophy of the duodenum in mice

Project description:RIPK1 is required in T cells with a history of CD4-expression to maintain intestinal homeostasis. We show that the pathology in the upper intestine is a result of conventional T cell apoptosis in absence of the RIPK1.

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Cooperation of TRADD- and RIPK1-dependent Cell Death Pathways in Maintaining Intestinal Homeostasis

Project description:Dysfunctional NF-kB signaling is critically involved in Inflammatory bowel disease (IBD). We investigated the mechanism by which RIPK1 and TRADD, two key mediators of NF-kB signaling, in mediating intestinal pathology using TAK1 IEC deficient model. We show that phosphorylation of TRADD by TAK1 modulates RIPK1-dependent apoptosis. TRADD and RIPK1 act cooperatively to mediate cell death mediated by TNF and TLR signaling. We demonstrate the pathological evolution from RIPK1-dependent ileitis to RIPK1- and TRADD-co-dependent colitis in TAK1 IEC deficient condition. Combined RIPK1 inhibition and TRADD knockout completely protect against intestinal pathology and lethality in TAK1 IEC KO mice. Furthermore, we identify distinctive microbiota dysbiosis biomarkers for RIPK1-dependent ileitis and TRADD-dependent colitis. These findings reveal the cooperation between RIPK1 and TRADD in mediating cell death and inflammation in IBD with NF-kB deficiency and suggest the possibility of combined RIPK1 kinase inhibition and TRADD knockout as a new therapeutic strategy for IBD.

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