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Nucleobase adducts bind MR1 and stimulate MR1-restricted T cells

ABSTRACT: Nucleobase adducts bind MR1 and stimulate MR1-restricted T cells

PROVIDER: PRJNA673154 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12931100.fastq.gz	Fastqsanger.gz
	SRR12931087.fastq.gz	Fastqsanger.gz
	SRR12931088.fastq.gz	Fastqsanger.gz
	SRR12931089.fastq.gz	Fastqsanger.gz
	SRR12931090.fastq.gz	Fastqsanger.gz

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Nucleobase adducts bind MR1 and stimulate MR1-restricted T cells

Project description:MR1T cells are a recently discovered class of T cells that recognize antigens presented by the MHC-I–related molecule MR1 in the absence of microbial infection. The nature of the self-antigens that stimulate MR1T cells remains unclear, hampering our understanding of their physiological role and therapeutic potential. By combining genetic, pharmacological, and biochemical approaches, we found that carbonyl stress and changes in nucleobase metabolism in target cells promote MR1T cell activation. Stimulatory compounds formed by carbonyl adducts of nucleobases were detected within MR1 molecules produced by tumor cells and their abundance and antigenicity were enhanced by drugs that induce carbonyl accumulation. Our data reveal carbonyl nucleobase adducts as MR1T cell antigens. Recognizing cells under carbonyl stress allows MR1T cells to monitor cellular metabolic changes with physiological and therapeutic implications.

2024-05-11 | GSE160366 | GEO

Transcriptome analysis of MR1 reactive T cells

Project description:MHC class I-related molecule MR1 presents riboflavin-derived microbial metabolites and folate-derivatives to mucosal-associated invariant T cells, but it is unknown whether MR1 can bind alternative antigens that stimulate other T cell lineages. Here we report that human T cells displaying diverse TCR-α and β chains recognize MR1-expressing cells in the absence of microbial ligands and respond to recombinant MR1 molecules loaded with antigens extracted from stimulatory targets. Transcriptome analysis revealed functional heterogeneity of MR1-reactive T cells (MR1T cells), which displayed differential expression of various transcription factors regulating T cell polarization, proliferation and apoptosis. Accordingly, MR1T cells displayed multiple profiles of chemokine receptor expression and secreted variable combinations of cytokines and growth factors, suggesting a diversity of immunological roles across numerous tissues. Functionally, MR1T cells were capable of inducing dendritic cell maturation and stimulating anti-microbial responses in intestinal epithelial cells. These data demonstrate that MR1 presents endogenous antigens to a novel population of functionally diverse human T cells.

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Effect of 4.25% PD fluid treatment on the peritoneum of MR1+/+ C57BL/6J and MR1-/- C57BL/6J mice

Project description:Mr1 knockout (Mr1−/−) mice, in which thymic cells lose the ability to promote the development of mature Mucosal-associated invariant T (MAIT) cells, induced systemic MAIT cell depletion. MAIT cells often exhibit altered functions during fibrosis and inflammatory diseases. Here we used intraperitoneal injections of 4.25% PD fluid (0.1 mL/g) daily for six weeks to mimic peritoneal dialysis (PD) related fibrosis in mice, and investigated whether Mr1 knockout could ameliorated PD-induced changes in peritoneal transcriptome. We analyzed bulk RNA-seq of peritoneums from Mr1+/+ + PBS group (n=3), Mr1+/+ + PD group (n=3), Mr1-/- + PBS group (n=2), and Mr1-/- + PD group (n=2), and demonstrated that Mr1 knockout could ameliorated PD-induced activation in fibrosis, hyperglycolysis, and mTORC1 signalings. In addition, the activation scores of these pathways are positively correlated with each other.

2024-12-06 | GSE279547 | GEO

scRNA-sequencing of non-neuron cells from hippocampus (HP) of 7 months old Mr1+/+ and Mr1-/- mice.

Project description:The purpose of this experiment is to examine the cellular and molecular changes in the microglia and other non-neuron cells in the hippocampus of 7 month old Mr1+/+ and Mr1-/- mice.

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Project description:Plaques are a hallmark feature of Alzheimer’s disease (AD). We found that the loss of mucosal-associated invariant T (MAIT) cells and its antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting dystrophic neurites. Brain tissue from 5XFAD mice and those that are MR1-deficient (MR1 KO), were analyzed for dystrophic neurites, amyloid plaques, and synapses via immunofluorescence, RNA sequencing, ELISA, and Western blot. In 8-month-old 5XFAD/MR1 KO mice, there was reduced expression of LAMP1, Ubiquitin, and n-terminal APP in the hippocampus as compared to 5XFAD mice (p < 0.05). 5XFAD/MR1 KO mice also had less insoluble Aβ40 (p < 0.001) and higher levels of PSD95 (p < 0.01) in the hippocampus. Our data contribute additional mechanistic insight into the detrimental role of the MR1/MAIT cell axis in AD pathology development.

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2022-07-12 | GSE197166 | GEO

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Project description:Mucosal-Associated Invariant T cells (MAIT cells) have a unique specificity for the microbial metabolite 5-OP-RU presented by the non-classical presentation molecule MR1. Upon activation, they release cytotoxic mediators and engage an antimicrobial activity. As a subset of T lymphocytes, MAIT development occurs in the thymus where they acquire their effector phenotype under the control of the key transcription factor ZBTB16. This particular maturation process is in contrast with conventional T cells that egress the thymus with a naive phenotype before populating the secondary lymphoid organs, and the molecular events driving the MAIT lineage decision are poorly known. In the present work, we evaluated the transcriptional events and the role of the slam-SAP pathway on the lineage decision of MR1-restricted T cells by single cell RNAseq. MAIT cells undergoing positive selection were FACS-sorted with a MR1:5-OP-RU labeled tetramer, from thymus of wild-type and sapKO mice. Their transcriptomes were captured using a 10x chromium system.

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