Evidence map›Paper›PMID 35164552›Full record

ArticlemBio2021

Augmentation of the Riboflavin-Biosynthetic Pathway Enhances Mucosa-Associated Invariant T (MAIT) Cell Activation and Diminishes Mycobacterium tuberculosis Virulence.

Ruchi Jain Dey, Bappaditya Dey, Melanie Harriff, Elizabeth T Canfield, David M Lewinsohn, William R Bishai

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Avoidance of MAIT cells is an essential determinant ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Review
  6. CD8+ lymphocytes in immunity against tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  7. Review
  8. Review
  9. A dual role for PGLYRP1 in host defense and immune regulation duringbioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Role of MHC class I pathways inFrontiers in cellular and infection microbiology · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ruchi Jain DeyCenter for Tuberculosis Research, Johns Hopkins University School of Medicinegrid.471401.7, Baltimore, Maryland, USA.
Bappaditya DeyCenter for Tuberculosis Research, Johns Hopkins University School of Medicinegrid.471401.7, Baltimore, Maryland, USA.
Melanie HarriffVA Portland Health Care System, Portland, Oregon, USA.
Elizabeth T CanfieldDivision of Pulmonary and Critical Care Medicine, Oregon Health & Science University, Portland, Oregon, USA.
David M LewinsohnVA Portland Health Care System, Portland, Oregon, USA.
William R BishaiCenter for Tuberculosis Research, Johns Hopkins University School of Medicinegrid.471401.7, Baltimore, Maryland, USA.ORCID 0000-0002-8734-4118
Johns Hopkins University · USOregon Health & Science University · US

Funding

Mycobacterium tuberculosis Survival Regulatory GenesR01AI037856 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BISHAI, WILLIAM RAMSES · 1997 to 2020
$7.2M
GENE REGULATION AND VIRULENCE IN TB AND MACR01AI036973 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BISHAI, WILLIAM RAMSES · 1999 to 2014
$5.7M
Lung Resident, MR1-Restricted T Cells: Association with Differential Outcomes Following Exposure to M. TuberculosisR01AI134790 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI LEWINSOHN, DAVID M., WALZL, GERHARD · 2018 to 2022
$3.3M
Distinct pathways for MR1 antigen presentation upon infection with intracellular versus extracellular pathogensR01AI129976 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI HARRIFF, MELANIE J · 2017 to 2021
$1.9M
BLRD VA I01 BX000533CSRD VA I01 CX001562NIAID NIH HHS R01 AI036973NIAID NIH HHS R01 AI037856NIAID NIH HHS R01 AI129976NIAID NIH HHS R01 AI134790
6 · The paper itself

Abstract

Mucosa-associated invariant T (MAIT) cells play a critical role in antimicrobial defense. Despite increased understanding of their mycobacterial ligands and the clinical association of MAIT cells with tuberculosis (TB), their function in protection against Mycobacterium tuberculosis infection remains unclear. Here, we show that overexpressing key genes of the riboflavin-biosynthetic pathway potentiates MAIT cell activation and results in attenuation of M. tuberculosis virulence

Indexed as

Mucosal-Associated Invariant T CellsMycobacterium tuberculosisTuberculosisAnimalsBiosynthetic PathwaysLigandsMiceMice, Inbred C57BLMucous MembraneRiboflavinVirulenceLigandsRiboflavinBCGMAIT cellsmucosal immunityMycobacterium tuberculosisriboflavintuberculosistuberculosis vaccines

Identifiers

PMID35164552
PMCPMC8844931
OpenAlexW4212988890

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.