Evidence map›Paper›PMID 29356555›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

Riboflavin Metabolism Variation among Clinical Isolates of Streptococcus pneumoniae Results in Differential Activation of Mucosal-associated Invariant T Cells.

Nadine Hartmann, Curtis McMurtrey, Michelle L Sorensen, Megan E Huber, Regina Kurapova, Fadie T Coleman, Joseph P Mizgerd, William Hildebrand, Mitchell Kronenberg, David M Lewinsohn and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-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

34 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Avoidance of MAIT cells is an essential determinant ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. MAIT cells: Conserved watchers on the wall.The Journal of experimental medicine · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Nadine Hartmann1 La Jolla Institute for Allergy and Immunology, San Diego, California.
Curtis McMurtrey2 Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Michelle L Sorensen3 Department of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Megan E Huber3 Department of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Regina Kurapova3 Department of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Fadie T Coleman4 Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts; and.
Joseph P Mizgerd4 Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts; and.
William Hildebrand2 Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Mitchell Kronenberg1 La Jolla Institute for Allergy and Immunology, San Diego, California.
David M Lewinsohn3 Department of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.
Melanie J Harriff3 Department of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon.ORCID 0000-0002-1461-5351
Oregon Health & Science University · USBoston University · USLa Jolla Institute for Immunology · USUniversity of Oklahoma Health Sciences Center · US

Funding

BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3M
Pneumonia BiologyR35HL135756 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MIZGERD, JOSEPH P · 2017 to 2023
$6.6M
Lung-resident antibacterial heterotypic immunityR01AI115053 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MIZGERD, JOSEPH P · 2015 to 2023
$4.0M
Differentiation of subsets of NKT cellsR01AI071922 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2016 to 2020
$2.7M
The role of natural killer T cells in the innate response to lung infectionR01AI105215 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2014 to 2018
$2.2M
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
Recognition of Mtb-Infected Cells by Non-Classically Restritcted CD8+ T CellsI01BX000533 · VA · PORTLAND VA MEDICAL CENTER · PI LEWINSOHN, DAVID M. · 2011 to 2024
–
Mtb uptake and antigen presentation in human lung epithelial cellsIK2CX000538 · VA · PORTLAND VA MEDICAL CENTER · PI HARRIFF, MELANIE J · 2012 to 2016
–
BLRD VA I01 BX000533CSRD VA IK2 CX000538NHLBI NIH HHS R35 HL135756NHLBI NIH HHS T32 HL007035NIAID NIH HHS R01 AI071922NIAID NIH HHS R01 AI105215NIAID NIH HHS R01 AI115053NIAID NIH HHS R01 AI129976
6 · The paper itself

Abstract

Streptococcus pneumoniae is an important bacterial pathogen that causes a range of noninvasive and invasive diseases. The mechanisms underlying variability in the ability of S. pneumoniae to transition from nasopharyngeal colonization to disease-causing pathogen are not well defined. Mucosal-associated invariant T (MAIT) cells are prevalent in mucosal tissues such as the airways and are believed to play an important role in the early response to infection with bacterial pathogens. The ability of MAIT cells to recognize and contain infection with S. pneumoniae is not known. In the present study, we analyzed MAIT-cell responses to infection with clinical isolates of S. pneumoniae serotype 19A, a serotype linked to invasive pneumococcal disease. We found that although MAIT cells were capable of responding to human dendritic and airway epithelial cells infected with S. pneumoniae, the magnitude of response to different serotype 19A isolates was determined by genetic differences in the expression of the riboflavin biosynthesis pathway. MAIT-cell release of cytokines correlated with differences in the ability of MAIT cells to respond to and control S. pneumoniae in vitro and in vivo in a mouse challenge model. Together, these results demonstrate first that there are genetic differences in riboflavin metabolism among clinical isolates of the same serotype and second that these likely determine MAIT-cell function in response to infection with S. pneumoniae. These differences are critical when considering the role that MAIT cells play in early responses to pneumococcal infection and determining whether invasive disease will develop.

Indexed as

AnimalsCytokinesDendritic CellsGene Expression Regulation, BacterialHost-Pathogen InteractionsHumansMice, Mutant StrainsPhagocytosisRespiratory MucosaRiboflavinStreptococcus pneumoniaeT-LymphocytesCytokinesRiboflavin

Identifiers

PMID29356555
PMCPMC6002660
OpenAlexW2806579973

What OpenQuestion holds

Textmetadata
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.