Evidence map›Paper›PMID 21628519›Full record

ArticleInfection and immunity2011

CD1d-independent activation of invariant natural killer T cells by staphylococcal enterotoxin B through major histocompatibility complex class II/T cell receptor interaction results in acute lung injury.

Sadiye Amcaoglu Rieder, Prakash Nagarkatti, Mitzi Nagarkatti

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Pathogens (Basel, Switzerland) · 2024
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. TBAScientific reports · 2019
    Article
  10. Article
  11. Review
  12. Review
  13. Resveratrol-Mediated Attenuation ofFrontiers in microbiology · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Sadiye Amcaoglu RiederDepartment of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29209, USA.
Prakash Nagarkatti
Mitzi Nagarkatti
University of South Carolina · US

Funding

Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
TCDD-INDUCED APOPTOSIS EFFECT ON T CELLSR01ES009098 · NIEHS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI NAGARKATTI, PRAKASH S · 1999 to 2008
$2.2M
Estrogen-T cell InteractionsR01ES019313 · NIEHS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI, NAGARKATTI, PRAKASH S · 2010 to 2014
$1.5M
Cannabinoid-induced apoptosis in T cell regulationR01DA016545 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI NAGARKATTI, PRAKASH S. · 2003 to 2007
$1.2M
NCCIH NIH HHS P01 AT003961NCCIH NIH HHS P01-AT03961NIDA NIH HHS R01 DA016545NIDA NIH HHS R01-DA016545NIEHS NIH HHS R01 ES009098NIEHS NIH HHS R01 ES019313NIEHS NIH HHS R01ES019313-02NIEHS NIH HHS R01-ES09098
6 · The paper itself

Abstract

There are two important mechanisms of activation of invariant natural killer T cells (iNKT cells) by microbes: direct activation of the invariant T-cell receptor (TCR) by microbial glycolipids presented by CD1d and indirect activation, mediated by the responses of antigen-presenting cells to microbes. In this study, we provide evidence for a novel CD1d-independent direct activation of iNKT cells involving a microbial protein superantigen presented in the context of major histocompatibility complex class II (MHC-II), which plays a critical role in pathogenesis, thereby redefining the role of iNKT cells. Intranasal exposure to staphylococcal enterotoxin B (SEB) in C57BL/6 wild-type mice caused acute lung injury (ALI) characterized by vascular leak, cytokine storm, and infiltration of mononuclear cells in the lungs. In contrast, the vascular leak and inflammation were decreased by ~50% in NKT cell-deficient Jα18(-/-) and CD1d(-/-) mice following SEB exposure, which was reversed following adoptive transfer of iNKT cells into CD1d(-/-) mice. In vitro, SEB could directly stimulate iNKT cells in a CD1d-independent manner via MHC-II/TCR interaction, specifically involving Vβ8. These studies not only demonstrate that iNKT cells can be activated directly by a bacterial protein superantigen independent of CD1d but also indicate that in addition to the conventional T cells, iNKT cells play a critical role in SEB-mediated ALI.

Indexed as

Lymphocyte ActivationAcute Lung InjuryAnimalsAntigens, CD1dCapillary PermeabilityCytokinesEnterotoxinsFemaleHistocompatibility Antigens Class IILeukocytes, MononuclearMiceMice, Inbred C57BLNatural Killer T-CellsReceptors, Antigen, T-CellAntigens, CD1dCd1d1 protein, mouseCytokinesenterotoxin B, staphylococcalEnterotoxinsHistocompatibility Antigens Class IIReceptors, Antigen, T-Cell

Identifiers

PMID21628519
PMCPMC3147567
OpenAlexW2104743286

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.