Human MAIT cells exit peripheral tissues and re-circulate via lymph in steady state conditions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA416130 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6231080.fastq.gz | Fastqsanger.gz | |||
| SRR6231081.fastq.gz | Fastqsanger.gz | |||
| SRR6231082.fastq.gz | Fastqsanger.gz | |||
| SRR6231083.fastq.gz | Fastqsanger.gz | |||
| SRR6231084.fastq.gz | Fastqsanger.gz |
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Project description:Mucosal-associated invariant T (MAIT) cells recognize bacterial metabolites as antigen and are found in blood and tissues, where they are poised to contribute to barrier immunity. Recent data demonstrate that MAIT cells located in mucosal barrier tissues are functionally distinct from their blood counterparts, but the relationship and circulation of MAIT cells between blood and different tissue compartments remains poorly understood. Previous studies raised the possibility that MAIT cells do not leave tissue and may either be retained or undergo apoptosis. To directly address if human MAIT cells exit tissues, we collected human donor-matched thoracic duct lymph and blood and analyzed MAIT cell phenotype, transcriptome and TCR diversity by RNAseq.
2018-03-26 | GSE106288 | GEO
Project description:Mucosal-associated invariant T cells (MAIT cells) recognize bacterial metabolites as antigen and are found in blood and tissues, where they are poised to contribute to barrier immunity. Recent data demonstrate that MAIT cells located in mucosal barrier tissues are functionally distinct from their blood counterparts, but the relationship and circulation of MAIT cells between blood and different tissue compartments remains poorly understood. Previous studies raised the possibility that MAIT cells do not leave tissue and may either be retained or undergo apoptosis. To directly address if human MAIT cells exit tissues, we collected human donor-matched thoracic duct lymph and blood and analyzed MAIT cell phenotype, transcriptome, and T cell receptor (TCR) diversity by flow cytometry and RNA sequencing. We found that MAIT cells were present in the lymph, despite being largely CCR7- in the blood, thus indicating that MAIT cells in the lymph migrated from tissues and were capable of exiting tissues to recirculate. Importantly, MAIT cells in the lymph and blood had highly overlapping clonotype usage but distinct transcriptome signatures, indicative of differential activation states.
| S-EPMC5928862 | biostudies-literature
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 | GSE145778 | GEO
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
Project description:Transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection
| PRJNA608200 | ENA
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
Project description:Tissue repair processes maintain proper organ function following mechanical or infection related damage. In addition to anti-bacterial properties, MAIT cells express a tissue repair transcriptomic program and promote skin wound healing when expanded. Herein, we use a human‑like full‑thickness skin excision mouse model to assess the underlying mechanisms of MAIT cell tissue repair function. Single-cell RNAseq analysis suggests that skin MAIT cells already express a repair program at steady state. Following skin excision, MAIT cells promote keratinocyte proliferation thereby accelerating healing. Using skin grafts, parabiosis and adoptive transfer experiments, we show that MAIT cells migrate into the wound from other tissues in a TCR independent but CXCR6 dependent manner. Amphiregulin secreted by MAIT cells following excision promotes wound healing. The repair function is independent of sustained TCR stimulation. Overall, our study provides mechanistic insight into MAIT cell wound healing function in the skin.
2023-01-10 | GSE207348 | GEO
Project description:Although mucosal associated invariant T (MAIT) cells provide rapid, innate-like responses, they are not pre-set and memory-like responses have been described for MAIT cells following infections. The importance of metabolism for controlling these responses, however, is unknown. Following pulmonary immunization with a Salmonella vaccine strain, mouse MAIT cells expanded as separate CD127-Klrg1+ and CD127+Klrg1- antigen-adapted populations that differed for their transcriptome, function and localization in lung tissue. These populations remained altered from steady-state for months as stable, separate MAIT cell lineages with enhanced effector programs and divergent metabolism. CD127+ MAIT cells engaged in an energetic, mitochondrial metabolic program, which was critical for their maintenance and IL-17A synthesis. This program was supported by high fatty acid uptake and mitochondrial oxidation and relied on highly polarized mitochondria and autophagy. After vaccination, CD127+ MAIT cells protected mice against Streptococcus pneumoniae infection. In contrast, Klrg1+ MAIT cells had dormant, but ready-to-respond mitochondria and depended instead on Hif1a-driven glycolysis. They responded vigorously to cytokines and participated in protection from influenza virus. These metabolic dependencies may enable tuning of memory-like MAIT cell responses for vaccinations and immunotherapies.
2023-03-29 | GSE226524 | GEO
Project description:Bcl11b binding and transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection
| PRJNA608197 | ENA
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