ArticlePLoS pathogens2025
Disruption of riboflavin biosynthesis in mycobacteria establishes riboflavin pathway intermediates as key precursors of MAIT cell agonists.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Human neonatal MR1T cells have more diverse TCR repertoires but reduced bacterial recognition than adult MR1T cells.Nature communications · 2026Article
- Sorting endosomes play key roles in presentation of Mycobacterium tuberculosis-derived ligands to MAIT cells.Scientific reports · 2026Article
- A miniaturized MR1 metabolite display system with native-like protein features.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mutations outside the MR1 antigen binding groove differentially inhibit presentation of exogenous antigens.The Journal of biological chemistry · 2026Article
- Sorting endosomes play key roles in presentation ofbioRxiv : the preprint server for biology · 2025Article
- CD4+ mucosal-associated invariant T cells express highly diverse T cell receptors.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The Crosstalk BetweenCells · 2025Review
- Human Neonatal MR1T Cells Have Diverse TCR Usage, are Less Cytotoxic and are Unable to Respond to Many Common Childhood Pathogens.bioRxiv : the preprint server for biology · 2025Article
- Flavin and deazaflavin biosynthesis in mycobacteria: relevance to physiology, implications for drug discovery, MR-1 antigenicity, and vaccine development.Frontiers in immunology · 2025Review
- Proteomic insights into mycobacterial responses to elevated riboflavin reveal a role for flavin-sequestering proteins in flavin homeostasis.Frontiers in tuberculosis · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Mucosal-associated invariant T (MAIT) cells exhibit an intrinsic ability to recognize and respond to microbial infections. The semi-invariant antigen recognition receptor of MAIT cells specifically detects the non-polymorphic antigen-presenting molecule, major histocompatibility complex class I-related protein 1 (MR1), which primarily binds riboflavin-derived metabolites of microbial origin. To further interrogate the dependence of these antigens on riboflavin biosynthesis in mycobacteria, we deleted individual genes in the riboflavin biosynthesis pathways in Mycobacterium smegmatis (Msm) and Mycobacterium tuberculosis (Mtb) and evaluated the impact thereof on MAIT cell activation. Blocking the early steps of the pathway by deletion of RibA2 or RibG profoundly reduced, but did not completely ablate, MAIT cell activation by Msm or Mtb, whereas deletion of RibC, which catalyzes the last step in the pathway, had no significant effect. Interestingly, deletion of the lumazine synthase (RibH) specifically enhanced MAIT cell recognition of Mtb whereas loss of lumazine synthase activity had no impact on MAIT cell activation by Msm. MAIT cell activation by Msm was likewise unaffected by blocking the production of the MAIT cell antagonist, Fo (by inhibiting its conversion from the riboflavin pathway intermediate, 5-amino-6-D-ribitylaminouracil (5-A-RU), through the deletion of fbiC). Together, these results confirm a central role for 5-A-RU in generating mycobacterial MR1 ligands and reveal similarities and differences between Msm and Mtb in terms of the impact of riboflavin pathway disruption on MAIT cell activation.
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