ArticleThe Journal of experimental medicine2025
Cigarette smoke components modulate the MR1-MAIT axis.
Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Review
- Comparative analysis of clinically approved lipid nanoparticles for intranasal siRNA delivery against SARS-CoV-2.Drug delivery and translational research · 2026Article
- ACAT1-Mediated SP1-K694 Lactylation Promotes M1 Macrophage Polarization via TREM1 Transcription in COPD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The MHC-I related protein 1 MR1 can bind host purine catabolites.The Journal of biological chemistry · 2026Article
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.Scientific reports · 2026Article
- Allelic variation alters expression and antigen presentation of MR1 allomorphs.The Journal of biological chemistry · 2026Article
- Article
- Mutations outside the MR1 antigen binding groove differentially inhibit presentation of exogenous antigens.The Journal of biological chemistry · 2026Article
- The antigen-presenting molecule MR1 binds host-generated riboflavin catabolites.The Journal of experimental medicine · 2026Article
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.bioRxiv : the preprint server for biology · 2026Article
- Global, regional, and 204 countries burden of disease attributed to secondhand smoke-related COPD, 1990-2021: A secondary data analysis of the Global Burden of Disease Study 2021.Tobacco induced diseases · 2026Article
- Smoking-induced HLA-DQA1 overexpression in T cells: a novel pathway in thyroid eye disease development.Frontiers in immunology · 2026Article
- Development of αβ and γδ T Cells in the Thymus and Methods of Analysis.International journal of molecular sciences · 2025Review
- Mucosal-Associated Invariant T Cells: Origins, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- MAIT cells promote cancer progression and regulatory T cell accumulation in bladder tumor microenvironment.Journal for immunotherapy of cancer · 2025Article
- Molecular Insights Into MR1-Mediated T Cell Immunity: Lessons Learned and Unanswered Questions.Immunological reviews · 2025Review
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
Tobacco smoking is prevalent across the world and causes numerous diseases. Cigarette smoke (CS) compromises immunity, yet little is known of the components of CS that impact T cell function. MR1 is a ubiquitous molecule that presents bacterial metabolites to MAIT cells, which are highly abundant in the lungs. Using in silico, cellular, and biochemical approaches, we identified components of CS that bind MR1 and impact MR1 cell surface expression. Compounds, including nicotinaldehyde, phenylpropanoid, and benzaldehyde-related scaffolds, bound within the A' pocket of MR1. CS inhibited MAIT cell activation, ex vivo, via TCR-dependent and TCR-independent mechanisms. Chronic CS exposure altered MAIT cell phenotype and function and attenuated MAIT cell responses to influenza A virus infection in vivo. MR1-deficient mice were partially protected from the development of chronic obstructive pulmonary disease (COPD) features that were associated with CS exposure. Thus, CS can impair MAIT cell function by diverse mechanisms, and potentially contribute to infection susceptibility and disease exacerbations.
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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.