Evidence map›Paper›PMID 21555485›Full record

ArticleThe Journal of experimental medicine2011

Innate and cytokine-driven signals, rather than microbial antigens, dominate in natural killer T cell activation during microbial infection.

Manfred Brigl, Raju V V Tatituri, Gerald F M Watts, Veemal Bhowruth, Elizabeth A Leadbetter, Nathaniel Barton, Nadia R Cohen, Fong-Fu Hsu, Gurdyal S Besra, Michael B Brenner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 269 citations in OpenAlex.

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  18. Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023
    Review
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  20. Article

123 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Manfred BriglDepartment of Pathology, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. mbrigl@rics.bwh.harvard.edu
Raju V V Tatituri
Gerald F M Watts
Veemal Bhowruth
Elizabeth A Leadbetter
Nathaniel Barton
Nadia R Cohen
Fong-Fu Hsu
Gurdyal S Besra
Michael B Brenner
Harvard University · USBrigham and Women's Hospital · USUniversity of Birmingham · GBWashington University in St. Louis · US

Funding

The impact of HIV viral diversity and cellular immunity on HIV pathogenesisP30AI060354 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ROBERT A. PARKER · 2004 to 2026
$94.4M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
YOGA LIFESTYLE INTERVENTION REDUCES BLOOD PRESSURE IN HIV-INFECTED ADULTSP41RR000954 · NCRR · WASHINGTON UNIVERSITY · PI GROSS, MICHAEL L · 1985 to 2011
$16.0M
PHOSPHOLIPID-DERIVED MEDIATORS AND INSULIN SECRETIONR37DK034388 · NIDDK · WASHINGTON UNIVERSITY · PI TURK, JOHN W · 1993 to 2010
$4.9M
T LYMPOHOCYTE RECOGNITIONR01AI028973 · NIAID · DANA-FARBER CANCER INSTITUTE · PI BRENNER, MICHAEL B. · 1990 to 2014
$4.5M
CD1d-restricted T Cell Self-antigens and InfectionR01AI063428 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B. · 2005 to 2015
$3.9M
T LYMPHOCYTE RECOGNITIONR37AI028973 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B · 1995 to 2004
$1.7M
CD1d-restricted NKT cells in microbial infectionK08AI077795 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BRIGL, MANFRED · 2008 to 2012
$782k
CD1d and NKT Cell Activation and Function in InfectionR56AI063428 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B. · 2010 to 2010
$433k
NCRR NIH HHS P41 RR000954NCRR NIH HHS P41-RR-00954NIAID NIH HHS AI028973NIAID NIH HHS AI063428NIAID NIH HHS AI077795NIAID NIH HHS K08 AI077795NIAID NIH HHS P30 AI060354NIAID NIH HHS R01 AI028973NIAID NIH HHS R01 AI063428NIAID NIH HHS R37 AI028973NIAID NIH HHS R56 AI063428NIDDK NIH HHS P60 DK020579NIDDK NIH HHS P60-DK-20579NIDDK NIH HHS R37 DK034388NIDDK NIH HHS R37-DK-34388
6 · The paper itself

Abstract

Invariant natural killer T cells (iNKT cells) are critical for host defense against a variety of microbial pathogens. However, the central question of how iNKT cells are activated by microbes has not been fully explained. The example of adaptive MHC-restricted T cells, studies using synthetic pharmacological α-galactosylceramides, and the recent discovery of microbial iNKT cell ligands have all suggested that recognition of foreign lipid antigens is the main driver for iNKT cell activation during infection. However, when we compared the role of microbial antigens versus innate cytokine-driven mechanisms, we found that iNKT cell interferon-γ production after in vitro stimulation or infection with diverse bacteria overwhelmingly depended on toll-like receptor-driven IL-12. Importantly, activation of iNKT cells in vivo during infection with Sphingomonas yanoikuyae or Streptococcus pneumoniae, pathogens which are known to express iNKT cell antigens and which require iNKT cells for effective protection, also predominantly depended on IL-12. Constitutive expression of high levels of IL-12 receptor by iNKT cells enabled instant IL-12-induced STAT4 activation, demonstrating that among T cells, iNKT cells are uniquely equipped for immediate, cytokine-driven activation. These findings reveal that innate and cytokine-driven signals, rather than cognate microbial antigen, dominate in iNKT cell activation during microbial infections.

Indexed as

AnimalsAntigens, BacterialCytokinesFemaleGalactosylceramidesInterferon-gammaInterleukin-12LigandsLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicNatural Killer T-CellsPhosphorylationSignal TransductionSpectrometry, Mass, Electrospray Ionizationalpha-galactosylceramideAntigens, BacterialCytokinesGalactosylceramidesInterferon-gammaInterleukin-12LigandsSTAT4 Transcription Factor

Identifiers

PMID21555485
PMCPMC3173255
OpenAlexW2102785691

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.