ArticleeLife2020
Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Des-O-Methyllasiodiplodin Isolated fromACS omega · 2026Article
- Mucosal-associated invariant T (MAIT) cells are reduced and dysfunctional in acute melioidosis.Scientific reports · 2026Article
- Signal Transducer and Activator of Transcription (STAT) Proteins Regulate Mucosal-Associated Invariant T (MAIT) Cell Function.Immunology · 2026Article
- Protective role of mucosa-associated invariant T cells in sepsis-related liver injury.Frontiers in immunology · 2026Article
- Synergistic TCR-independent action of IL-33 and IL-12 drive a potent IFNγ secretory program in human circulating MAIT cells with immunomodulatory properties.Frontiers in immunology · 2026Article
- Developmental features and unique characteristics of peptide-specific PLZFNature communications · 2025Article
- Hantaan virus infection induces human mucosal-associated invariant T cell pyroptosis through IRE1α pathway.Communications biology · 2025Article
- Distinct MAIT cell phenotypes associated with sepsis clinical outcome in emergency department patients.Clinical & translational immunology · 2025Article
- The Emerging Roles and Therapeutic Potential of Unconventional T Cells in Sepsis.Journal of inflammation research · 2025Review
- Conventional and unconventional T-cell responses contribute to the prediction of clinical outcome and causative bacterial pathogen in sepsis patients.Clinical and experimental immunology · 2024Article
- Review
- Destabilisation of T cell-dependent humoral immunity in sepsis.Clinical science (London, England : 1979) · 2024Review
- Translatome analyses by bio-orthogonal non-canonical amino acid labeling reveal that MR1-activated MAIT cells induce an M1 phenotype and antiviral programming in antigen-presenting monocytes.Frontiers in immunology · 2023Article
- Mucosal-Associated Invariant T cells exhibit distinct functional signatures associated with protection against typhoid fever.Cellular immunology · 2022Article
- A tRNA modifying enzyme as a tunable regulatory nexus for bacterial stress responses and virulence.Nucleic acids research · 2022Article
- Human MAIT Cells Respond toMicroorganisms · 2022Article
- Riboflavin Attenuates Influenza Virus Through Cytokine-Mediated Effects on the Diversity of the Gut Microbiota in MAIT Cell Deficiency Mice.Frontiers in microbiology · 2022Article
- Functional inactivation of pulmonary MAIT cells following 5-OP-RU treatment of non-human primates.Mucosal immunology · 2021Article
- Title of article: Mucosal-associated invariant T cells in lung diseases.International immunopharmacology · 2021Review
- Nicotinamide Mononucleotide Alleviates Hyperosmolarity-Induced IL-17a Secretion and Macrophage Activation in Corneal Epithelial Cells/Macrophage Co-Culture System.Journal of inflammation research · 2021Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis is a systemic inflammatory response to infection and a leading cause of death. Mucosal-associated invariant T (MAIT) cells are innate-like T cells enriched in mucosal tissues that recognize bacterial ligands. We investigated MAIT cells during clinical and experimental sepsis, and their contribution to host responses. In experimental sepsis, MAIT-deficient mice had significantly increased mortality and bacterial load, and reduced tissue-specific cytokine responses. MAIT cells of WT mice expressed lower levels of IFN-γ and IL-17a during sepsis compared to sham surgery, changes not seen in non-MAIT T cells. MAIT cells of patients at sepsis presentation were significantly reduced in frequency compared to healthy donors, and were more activated, with decreased IFN-γ production, compared to both healthy donors and paired 90-day samples. Our data suggest that MAIT cells are highly activated and become dysfunctional during clinical sepsis, and contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.