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Blocking MAIT cell activation can modulate macrophage gene signature during liver fibrosis regression

ABSTRACT: Blocking MAIT cell activation can modulate macrophage gene signature during liver fibrosis regression

PROVIDER: PRJNA762314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15840400_1.fastq.gz	Fastqsanger.gz
	SRR15840400_2.fastq.gz	Fastqsanger.gz
	SRR15840401_1.fastq.gz	Fastqsanger.gz
	SRR15840401_2.fastq.gz	Fastqsanger.gz
	SRR15840402_1.fastq.gz	Fastqsanger.gz

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Blocking MAIT cell activation can modulate macrophage gene signature during liver fibrosis regression

Project description:Exploratory RNA sequencing of pro-inflammatory (Ly6C high) and resolutive (Ly6C low) macrophages in mouse liver during fibrosis regression. Mice were treated with a MAIT antagonist or its control vehicle for 2 days after the last CCl4 injection. Ly6C high and Ly6C low macrophages were sorted by ARIA III.

2023-02-10 | GSE183906 | GEO

Gene expression profiles of MAIT cells, MAIT-iPSCs, hiPSCs, hESCs, and reMAIT cells

Project description:To show the similarity among MAIT-iPSCs, hiPSCs and hESCs and the gradual change of global gene expression of reMAIT cells along with differentiation, this experiment was designed. MAIT cells, MAIT-iPSCs, hiPSCs, hESCs, MAIT cells, and reMAIT cells at the several differerent stages of differentiation were collected. Then, they were applied in this experiment.

2013-03-21 | E-GEOD-44559 | biostudies-arrayexpress

Microarray expression profiling of NKT and MAIT subsets in different organs of B6-MAIT/CAST mice.

Project description:MAIT cells (MAITs) represent an abundant T lymphocyte subset with unique specificity for microbial metabolites presented by the MHC-1b molecule, MR1. MAIT conservation along evolution indicates important, non-redundant functions, but their low frequency in mice has hampered their detailed characterization. Here, we performed a transcriptomic analysis of murine MAITs in comparison with NKT subsets and with mainstream T cells in spleen and peripheral organs of B6-MAIT/CAST mice expressing a Rorc-GFP transgene. MAIT and NKT cells have been FACS-sorted after tetramer staining (MR1:5-OP-RU Tet+ for MAIT, CD1d:PBS57Tet+ for NKT), and 1/17 subsetting based on the expression of Rorc.

2018-12-03 | E-MTAB-7133 | biostudies-arrayexpress

MAIT cell RNA sequencing

Project description:Obesity underpins the development of numerous chronic diseases such as type II diabetes mellitus. It is well established that obesity negatively alters immune cell frequencies and functions. Mucosal Associated Invariant T (MAIT) cells are a population of innate T cells, which we have previously reported are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in their IFN-gamma production, which is a critical effector function of MAIT cells in host defence. Hence there is increased urgency to characterise the key molecular mechanisms that drive MAIT cell effector functions, and to identify those which are impaired in the obesity setting. In this study, we found that MAIT cells significantly upregulate their rates of glycolysis upon activation in an mTORC1 dependent manner and this is essential for MAIT cell IFN-g production. Furthermore, we show that mTORC1 activation is dependent on amino acid transport via SLC7A5. In obese patients, using RNA sequencing, Seahorse analysis and a series of in vitro experiments, we demonstrate that MAIT cells isolated from obese adults display defective glycolytic metabolism, mTORC1 signalling and SLC7A5 amino acid transport. Collectively our data details the intrinsic metabolic pathways controlling MAIT cell cytokine production and highlights mTORC1 as an important metabolic regulator that is impaired in obesity, leading to altered MAIT cell responses. We report on MAIT cells isolated from lean and obese adults

2019-04-16 | GSE126169 | GEO

Single-cell RNA sequencing of MAIT cells from young and aged mice

Project description:In this study, we performed single-cell RNA sequencing (scRNA-seq) on MAIT cells extracted from the intestines of young and aged mice. For each age group, MAIT cells from five individual mice were pooled before sequencing.

2024-11-26 | E-MTAB-14483 | biostudies-arrayexpress

MAIT cell inhibition promotes liver fibrosis regression via macrophage phenotype reprogramming.

Project description:Recent data have shown that liver fibrosis can regress even at later stages of cirrhosis and shifting the immune response from pro-inflammatory towards a resolutive profile is considered as a promising option. The immune regulatory networks that govern the shift of the inflammatory phenotype and thus potential reversal of liver fibrosis are lesser known. Here we show that in precision-cut human liver slices obtained from patients with end-stage fibrosis and in mouse models, inhibiting Mucosal-Associated Invariant T (MAIT) cells using pharmacological or antibody-driven approaches, limits fibrosis progression and even regresses fibrosis, following chronic toxic- or non-alcoholic steatohepatitis (NASH)-induced liver injury. Mechanistic studies, combining RNA sequencing, in vivo functional studies (performed in male mice) and co-culture experiments indicate that disruption of the MAIT cell-monocyte/macrophage interaction results in resolution of fibrosis both by increasing the frequency of restorative Ly6Clo at the expenses of pro-fibrogenic Ly6Chi monocyte-derived macrophages and promoting an autophagic phenotype in both subsets. Thus, our data show that MAIT cell activation and the consequential phenotype shift of liver macrophages are important pathogenic features of liver fibrosis and could be targeted by anti-fibrogenic therapy.

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Microarray expression profiling of MAIT subsets isolated from thymus of B6-MAIT/CAST mice, as compared to single positive CD4 or CD8 conventional T cells.

Project description:In mice, contrary to conventional T cells, MAIT cells acquire a memory phenotype in the thymus in relation with Zbtb16 expression (Savage et al., 2008 ; Koay et al., 2016). To define phenotypic transcriptional signatures of MAIT subsets in the thymus, we analyzed by microarray the transcriptome of MAIT1 (MR1tet+RORgt+) and MAIT17 (MR1tet+RORgt+) as compared to conventional mature (TCRb+CD24lo) CD4+ and CD8+ single positive cells.

2019-07-01 | E-MTAB-7702 | biostudies-arrayexpress

MAIT cell project

Project description:MAIT cell project

| PRJNA637387 | ENA

Mapping H3K27ac in human MAIT cells

Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.

2021-03-22 | GSE145777 | GEO

Single-Cell Transcriptome Analysis of MAIT Cell Subsets from human normal intestine

Project description:Normal adjacent tissues from colorectal cancer patients were collected for MAIT cell sorting. Sorted MAIT cells from seven individual donors were pooled together. Single-cell RNA sequencing libraries were prepared using the Chromium 5' Single Cell Gene Expression Kit (10x Genomics), following the manufacturer's protocol. Sequencing was performed on a NextSeq 500 platform (Illumina).

2024-11-26 | E-MTAB-14482 | biostudies-arrayexpress

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