bims-maitce Biomed News
on MAIT cells
Issue of 2025–09–21
two papers selected by
Andy E. Hogan, Maynooth University



  1. J Immunother Cancer. 2025 Sep 15. pii: e012496. [Epub ahead of print]13(9):
       BACKGROUND: Mucosa-associated invariant T (MAIT) cells represent a unique population of innate-like T lymphocytes capable of detecting non-peptide antigens in the context of monomorphic antigen-presenting molecules. Due to their abundance in barrier tissues, reactivity to local inflammatory cues, and cytotoxic and regulatory functions, MAIT cells are poised to shape the dynamics of various tumor microenvironments. Growing evidence suggests that MAIT cells can exert protumor and/or antitumor effects in cancers arising from or metastasizing to mucosal tissues. However, MAIT cell roles in bladder cancer (BCa) remains unclear.
    METHODS: To begin to identify MAIT cells in BCa, we stained bladder tumor biopsies for T cell receptor (TCR) Vα7.2+ cells. We then refined a human MAIT cell signature, which enabled us to interrogate a bulk RNA sequencing dataset and conduct correlation analyses linking intratumoral MAIT cell abundance and mortality from BCa. To extend our work to an in vivo setting, we employed a clinically relevant mouse model in which Mr1 +/+ B6-MAITCAST (MAIT-sufficient) and Mr1 -/- B6-MAITCAST (MAIT-deficient) mice were exposed to N-butyl-N-(4-hydroxybutyl)nitrosamine, a chemical carcinogen associated with tobacco smoke. In additional experiments, MAIT cells were functionally removed through acetyl-6-formylpterin (Ac-6-FP) administration. Effector and regulatory cell types were phenotyped by flow cytometry, and BCa tumor burden and progression were assessed by MRI and/or H&E and Ki67 staining.
    RESULTS: TCR Vα7.2+ cells were readily detectable in several BCa biopsies, and our bioinformatic analyses correlated heavier MAIT cell presence in BCa tumors with poorer overall survival. Similarly, we found higher tumor burdens in Mr1+/+ B6-MAITCAST mice than in Mr1-/- or Ac-6-FP-treated animals. Bladder MAIT cells from tumor-bearing mice exhibited phenotypic MAIT17 bias based on transcription factors they harbored along with increased interleukin-17A and tumor necrosis factor-α production capacities upon stimulation. Finally, FoxP3+ regulatory T (Treg) cell frequencies were elevated in Mr1+/+ mouse bladder tumors, likely contributing to an immunosuppressive tumor microenvironment, a finding that could be recapitulated in our transcriptomic studies on human BCa.
    CONCLUSIONS: MAIT cells are abundant in BCa tumor microenvironments where they potentiate Treg cell accumulation and play protumor roles.
    Keywords:  Bladder Cancer; Cytokine; T cell; T regulatory cell - Treg; Tumor microenvironment - TME
    DOI:  https://doi.org/10.1136/jitc-2025-012496
  2. Clin Cosmet Investig Dermatol. 2025 ;18 2243-2257
       Background: Psoriasis is a chronic inflammatory skin disease involving dysregulated immune responses and complex genetic factors. This study combines single-cell RNA sequencing (scRNA-seq), gene expression profiling, and genetic analysis to explore cellular and molecular contributors to psoriasis.
    Methods: Single-cell RNA-seq data (n = 3 psoriasis, n = 2 control; GSE228421) were used for cell-type annotation and functional characterization. T cell subsets were analyzed for differentiation trajectories and cell-cell communication. Differentially expressed genes in mucosal-associated invariant T (MAIT) cells were evaluated by enrichment analysis. Candidate gene causality was tested via eQTL-based Mendelian randomization (MR) and supported by bulk RNA-seq validation.
    Results: MAIT cells were enriched in psoriatic lesions and exhibited strong intercellular interactions. Functional analyses revealed activation of IL6-JAK-STAT3 signaling, TNF-NFκB pathway, and glycolysis in MAIT cells. MR identified RPS20 as a protective factor (OR = 0.5994, p = 0.011) and PFN1 as a potential risk gene (OR = 1.7229, p = 0.037), with PFN1 highly expressed in MAIT cells. Colocalization analysis showed no significant genetic overlap between PFN1 expression and psoriasis risk. Metabolic profiling revealed differential pathway involvement in PFN1+ and PFN1- MAIT cells.
    Conclusion: Our integrative analysis highlights MAIT cells and PFN1 as likely contributors to psoriasis pathogenesis. These findings offer insights into immune and metabolic alterations, suggesting potential targets for therapeutic intervention.
    Keywords:  MAIT cells; PFN1; eQTL Mendelian randomization analysis; psoriasis; scRNA-seq
    DOI:  https://doi.org/10.2147/CCID.S535795