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A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (T cell RNA Seq dataset)

ABSTRACT: A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (T cell RNA Seq dataset)

PROVIDER: PRJNA614016 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11389214.fastq.gz	Fastqsanger.gz
	SRR11389215.fastq.gz	Fastqsanger.gz
	SRR11389216.fastq.gz	Fastqsanger.gz
	SRR11389217.fastq.gz	Fastqsanger.gz
	SRR11389218.fastq.gz	Fastqsanger.gz

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A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (Dendritic cell RNA Seq dataset)

Project description:A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (Dendritic cell RNA Seq dataset)

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A purine metabolic checkpoint that prevents autoimmunity and autoinflammation.

Project description:Still's disease, the paradigm of autoinflammation-cum-autoimmunity, predisposes for a cytokine storm with excessive T lymphocyte activation upon viral infection. Loss of function of the purine nucleoside enzyme FAMIN is the sole known cause for monogenic Still's disease. Here we discovered that a FAMIN-enabled purine metabolon in dendritic cells (DCs) restrains CD4+ and CD8+ T cell priming. DCs with absent FAMIN activity prime for enhanced antigen-specific cytotoxicity, IFNγ secretion, and T cell expansion, resulting in excessive influenza A virus-specific responses. Enhanced priming is already manifest with hypomorphic FAMIN-I254V, for which ∼6% of mankind is homozygous. FAMIN controls membrane trafficking and restrains antigen presentation in an NADH/NAD+-dependent manner by balancing flux through adenine-guanine nucleotide interconversion cycles. FAMIN additionally converts hypoxanthine into inosine, which DCs release to dampen T cell activation. Compromised FAMIN consequently enhances immunosurveillance of syngeneic tumors. FAMIN is a biochemical checkpoint that protects against excessive antiviral T cell responses, autoimmunity, and autoinflammation.

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A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (Dendritic cell RNA Seq dataset)

Project description:Mutations resulting in loss of FAMIN (C13orf31) cause systemic juvenile idiopathic arthritis and very early onset inflammatory bowel disease, while a common I254V substitution increases susceptibility to leprosy and Crohn’s disease. In this study, we compare mRNA transcriptional profiles of bone marrow-derived dendritic cells (DCs) from mice genetically engineered to express Faminp.254I (non-risk), Faminp.254V (risk variant) and Faminp.284R (mutant) at their endogenous loci. We also compare BMDCs from mice lacking FAMIN expression -/- (knockout, KO) with FAMIN+/+ (wild type, WT) mice.

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A purine metabolic checkpoint that prevents autoimmunity and autoinflammation (T cell RNA Seq dataset)

Project description:In this study, we investigate how FAMIN activity in dendritic cells determines the release of mediators that affect priming, activation and gene transcription of CD8+ T cells.

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Purine nucleoside phosphorylase enables dual metabolic checkpoints that prevent T cell immunodeficiency and TLR7-associated autoimmunity

Project description:Purine nucleoside phosphorylase (PNP) enables the breakdown and recycling of guanine nucleosides. PNP insufficiency in humans is paradoxically associated with both immunodeficiency and autoimmunity, but the mechanistic basis for these outcomes is incompletely understood. Here we identify two immune lineage-dependent consequences of PNP inactivation dictated by distinct gene interactions. During T cell development, PNP inactivation is synthetically lethal with down-regulation of the dNTP triphosphohydrolase SAMHD1. This interaction requires deoxycytidine kinase activity and is antagonized by microenvironmental deoxycytidine. In B lymphocytes and macrophages, PNP regulates Toll like receptor 7 signaling by controlling the levels of its (deoxy)guanosine nucleoside ligands. Overriding this regulatory mechanism promotes germinal center formation in the absence of exogenous antigen and accelerates disease in a mouse model of autoimmunity. This work reveals that one purine metabolism gene protects against immunodeficiency and autoimmunity via independent mechanisms operating in distinct immune lineages and identifies PNP as a novel metabolic immune checkpoint.

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Project description:Enterococcus faecalis is commonly isolated from different wound types. However, despite its prevalence, the pathogenic mechanisms of E. faecalis during wound infections remain poorly understood. We adopted an in vivo E. faecalis transposon sequencing and RNA sequencing approach to identify fitness determinants that are crucial for replication and persistence of E. faecalis during wound infections in a mouse model. We demonstrated that E. faecalis purine biosynthesis genes are important for replication as purine metabolites are low in wounds during the early phase of wound infections. Furthermore, we found that the E. faecalis MptABCD phosphotransferase system (PTS) involved in the uptake of galactose and mannose, is crucial for E. faecalis persistence in wounds, and that carbohydrate availability changes as the infection progresses. To understand how MptABCD PTS contributes to the reduced fitness observed during E. faecalis wound persistence, we performed an in vitro transcriptomic analysis using the galactose/mannose PTS gene deletion mutant (∆mptD). When mannose was the sole carbohydrate source, shikimate and purine biosynthesis genes in the ∆mptD mutant were downregulated compared to the isogenic wild-type strain, indicating that mannose transport is interconnected with shikimate and purine biosynthesis. Together, our results suggest that dynamic and temporal microenvironment changes at the wound site affects pathogenic requirements and mechanisms of E. faecalis during infections and raise the possibility of inhibiting purine biosynthesis and/or MptABCD PTS to control wound infections.

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