Evidence map›Paper›PMID 30282828›Full record

ArticleJCI insight2018

Mucosal-associated invariant and γδ T cell subsets respond to initial Mycobacterium tuberculosis infection.

Charles Kyriakos Vorkas, Matthew F Wipperman, Kelin Li, James Bean, Shakti K Bhattarai, Matthew Adamow, Phillip Wong, Jeffrey Aubé, Marc Antoine Jean Juste, Vanni Bucci and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 81 citations in OpenAlex.

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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

12 authors at 6 institutions in 3 countries.

Charles Kyriakos VorkasDivision of Infectious Diseases, Weill Cornell Medicine (WCM), New York, New York, USA.
Matthew F WippermanImmunology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center (MSKCC), New York, New York, USA.
Kelin LiDivision of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
James BeanImmunology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center (MSKCC), New York, New York, USA.
Shakti K BhattaraiDepartment of Bioengineering, University of Massachusetts, Dartmouth, North Dartmouth, Massachusetts, USA.
Matthew AdamowImmune Monitoring Core Facility, Ludwig Center for Cancer Immunotherapy, Sloan Kettering Institute, MSKCC, New York, New York, USA.
Phillip WongImmune Monitoring Core Facility, Ludwig Center for Cancer Immunotherapy, Sloan Kettering Institute, MSKCC, New York, New York, USA.
Jeffrey AubéDivision of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Marc Antoine Jean JusteGHESKIO Centers, Port-au-Prince, Haiti.
Vanni BucciDepartment of Bioengineering, University of Massachusetts, Dartmouth, North Dartmouth, Massachusetts, USA.
Daniel W FitzgeraldDivision of Infectious Diseases, Weill Cornell Medicine (WCM), New York, New York, USA.
Michael S GlickmanImmunology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center (MSKCC), New York, New York, USA.
Memorial Sloan Kettering Cancer Center · USKettering University · USUniversity of Massachusetts Dartmouth · USUniversity of North Carolina at Chapel Hill · USCornell University · USGheskio Centers · HT

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Viable but Nonculturable MtbU19AI111143 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI FITZGERALD, DANIEL W, GLICKMAN, MICHAEL S · 2014 to 2020
$48.6M
T32: Pathogenesis of Infectious Diseases Training ProgramT32AI007613 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ROY M. GULICK · 1999 to 2026
$8.8M
J. NRSA Training CoreTL1TR002386 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Genevieve Giny Fouda Amou ou · 2017 to 2026
$5.8M
Training in pharmacokinetic and pharmacodynamics research in HIV and tuberculosisD43TW010062 · FIC · WEILL MEDICAL COLL OF CORNELL UNIV · PI FITZGERALD, DANIEL W · 2015 to 2019
$1.8M
Global Health Research Training in HIV and TuberculosisK24AI098627 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI FITZGERALD, DANIEL W · 2012 to 2022
$1.8M
The role of Mucosal-associated invariant T (MAIT) cells during the innate immune response to Mycobacterium tuberculosisK08AI132739 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI VORKAS, CHARLES KYRIAKOS · 2018 to 2022
$921k
Mathematical modeling from metagenomics - minimizing risk of enteric infectionsR15AI112985 · NIAID · UNIVERSITY OF MASSACHUSETTS DARTMOUTH · PI BUCCI, VANNI · 2015 to 2015
$465k
FIC NIH HHS D43 TW010062NCATS NIH HHS TL1 TR002386NCI NIH HHS P30 CA008748NIAID NIH HHS K08 AI132739NIAID NIH HHS K24 AI098627NIAID NIH HHS R15 AI112985NIAID NIH HHS T32 AI007613NIAID NIH HHS U19 AI111143
6 · The paper itself

Abstract

Innate immune responses that control early Mtb infection are poorly understood, but understanding these responses may inform vaccination and immunotherapy strategies. Innate T cells that respond to conserved bacterial ligands such as mucosal-associated invariant T (MAIT) and γδ T cells are prime candidates to mediate these early innate responses but have not been examined in subjects who have been recently exposed to Mtb. We recruited a cohort living in the same household with an active tuberculosis (TB) case and examined the abundance and functional phenotypes of 3 innate T cell populations reactive to M. tuberculosis: γδ T, invariant NK T (iNKT), and MAIT cells. Both MAIT and γδ T cells from subjects with Mtb exposure display ex vivo phenotypes consistent with recent activation. However, both MAIT and γδ T cell subsets have distinct response profiles, with CD4+ MAIT and γδ T cells accumulating after infection. Examination of exposed but uninfected contacts demonstrates that resistance to initial infection is accompanied by robust MAIT cell CD25 expression and granzyme B production coupled with a depressed CD69 and IFNγ response. Finally, we demonstrate that MAIT cell abundance and function correlate with the abundance of specific gut microbes, suggesting that responses to initial infection may be modulated by the intestinal microbiome.

Indexed as

Immunity, InnateAdolescentAdultChildCohort StudiesDisease ResistanceFemaleGastrointestinal MicrobiomeHumansImmunity, MucosalIntestinal MucosaIntraepithelial LymphocytesLymphocyte ActivationMaleMiddle AgedMucosal-Associated Invariant T CellsImmunologyInfectious diseaseInnate immunityTuberculosis

Identifiers

PMID30282828
PMCPMC6237486
OpenAlexW2894861859

What OpenQuestion holds

Textmetadata
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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.