MAIT cells regulate NK cell mediated tumor immunity (NanoString)
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ABSTRACT:
PROVIDER: PRJNA742403 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This study reveals the dichotomous role of MAIT cells in regulating NK cell mediated anti-tumor immunity.
2021-07-06 | GSE179140 | GEO
Project description:This study reveals the dichotomous role of MAIT cells in regulating NK cell mediated anti-tumor immunity.
2021-07-06 | GSE179139 | GEO
Project description:MAIT cells regulate NK cell mediated tumor immunity (RNA-Seq)
| PRJNA742401 | ENA
Project description:The function of MR1-restricted mucosal-associated invariant T (MAIT) cells in tumor immunity is unclear. Here we show that MAIT cell-deficient mice have enhanced NK cell-dependent control of metastatic B16F10 tumor growth relative to control mice. Analyses of this interplay in human tumor samples reveal that high expression of a MAIT cell gene signature negatively impacts the prognostic significance of NK cells. Paradoxically, pre-pulsing tumors with MAIT cell antigens, or activating MAIT cells in vivo, enhances anti-tumor immunity in B16F10 and E0771 mouse tumor models, including in the context of established metastasis. These effects are associated with enhanced NK cell responses and increased expression of both IFN-γ-dependent and inflammatory genes in NK cells. Importantly, activated human MAIT cells also promote the function of NK cells isolated from patient tumor samples. Our results thus describe an activation-dependent, MAIT cell-mediated regulation of NK cells, and suggest a potential therapeutic avenue for cancer treatment.
| S-EPMC8346465 | biostudies-literature
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: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:Mucosal associated invariant T (MAIT) cells are lymphocytes that mediate tissue homeostasis and antimicrobial immunity. MAIT cells recognize microbial vitamin B-derived antigens (VitBAg) presented by MHC class I-related protein 1 (MR1). The cells that express MR1 and present VitBAg to MAIT cells remain unknown. We found that MR1 expression varies across tissues and cell types. Expression is regulated transcriptionally and induced by the tissue environment and microbiota. Depletion of MR1 in macrophages, dendritic cells and monocytes changed the composition of the microbiota and impaired MAIT cell responses against bacteria infection. Macrophages expressed the highest levels of MR1 and were the most efficient at capturing and presenting VitBAg to MAIT cells. We conclude that macrophages are key players in MR1 antigen presentation and MAIT cell immunity.
2025-12-08 | GSE306827 | GEO
Project description:Mucosal associated invariant T (MAIT) cells are lymphocytes that mediate tissue homeostasis and antimicrobial immunity. MAIT cells recognize microbial vitamin B-derived antigens (VitBAg) presented by MHC class I-related protein 1 (MR1). The cells that express MR1 and present VitBAg to MAIT cells remain unknown. We found that MR1 expression varies across tissues and cell types. Expression is regulated transcriptionally and induced by the tissue environment and microbiota. Depletion of MR1 in macrophages, dendritic cells and monocytes changed the composition of the microbiota and impaired MAIT cell responses against bacteria infection. Macrophages expressed the highest levels of MR1 and were the most efficient at capturing and presenting VitBAg to MAIT cells. We conclude that macrophages are key players in MR1 antigen presentation and MAIT cell immunity.
2025-12-08 | GSE306826 | GEO
Project description:Natural killer (NK) cells are primarily responsible for tumor surveillance, and their activation entirely depends on optimal metabolic signals. The adaptation of NK cell anti-tumor responses to nutritional stress is still poorly understood. Here, based on single-cell RNA sequencing, we discovered that dietary restriction (DR) enriches the rejuvenated subset of CD27+CD11b+ NK cells and improves their activation via Eomesodermin (Eomes), a transcription factor upregulated during DR treatment. Eomes reverses the differentiation of rejuvenated to senescent NK cells by antagonizing the T-bet-Zeb2 axis while improving chemotaxis and adhesion. Furthermore, DR increases the chromatin accessibility of Eomes to genes that regulate chemotaxis and adhesion in NK cells. To summarize, tumor control under dietary restriction requires Eomes-regulated NK cell anti-tumor immunity.
2024-01-01 | GSE249425 | GEO
Project description:Ischemic heart failure remains a major clinical challenge, underscoring the need to better understand post-infarction immune mechanisms and identify new therapeutic targets. Both innate and adaptive immunity contribute to adverse cardiac remodeling following myocardial infarction (MI), yet the role of cytotoxic cells such as natural killer (NK) cells remains poorly defined. Here, we show that after acute MI in mice, NK cells are recruited to the ischemic myocardium in a CCR2-dependent manner and become activated. Activated NK cells locally release granzyme B, promoting cardiomyocyte apoptosis, adverse ventricular remodeling, and impaired cardiac function. Genetic deletion or pharmacological depletion of NK cells reduces cardiomyocyte death, attenuates inflammation, limits myocardial injury, and improves cardiac function. In contrast, NK cell activation using an anti-NKG2A monoclonal antibody exacerbates ischemic heart failure. We further demonstrate that NK cells regulate bone marrow myelopoiesis through local GM-CSF production. Finally, we identify a distinct NK cellular and transcriptomic signature in human ischemic heart tissue at early stages. Together, these findings reveal a detrimental role for NK cells following acute MI and highlight NK cells as potential therapeutic targets to limit adverse cardiac remodeling.
2026-03-18 | GSE325257 | GEO