Evidence map›Paper›PMID 21458584›Full record

ReviewMicrobes and infection2011

Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis.

Samuel M Behar, Constance J Martin, Cláudio Nunes-Alves, Maziar Divangahi, Heinz G Remold

Abstract readReview
In one paragraph

Review in Microbes and infection, 2011. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Frontiers in immunology · 2021
    Article
  10. Article
  11. The Macrophage Response toFrontiers in cellular and infection microbiology · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. IFNγ-producing CD4Clinical and translational medicine · 2017
    Article
  18. Article
  19. Article
  20. PPE38 Protein ofFrontiers in cellular and infection microbiology · 2017
    Article
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

5 authors.

Samuel M BeharDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Smith Research Building, 1 Jimmy Fund Way, Boston, MA 02115, USA. sbehar@rics.bwh.harvard.edu
Constance J Martin
Cláudio Nunes-Alves
Maziar Divangahi
Heinz G Remold

Funding

Role of lipid mediators in host resistance to Mycobacterium tuberculosisR01AI072143 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI REMOLD, HEINZ GERNOT · 2007 to 2011
$2.1M
Antigen-specific CD8+ T cells and protective immunity to tuberculosisR01AI067731 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2006 to 2010
$2.0M
ROLE OF THE ALPHAE INTEGRIN IN IMMUNITY TO TUBERCULOSISR01AI047171 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2000 to 2004
$1.7M
A Novel Mechanism of Innate Immunity Against TBR01AI050216 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI REMOLD, HEINZ GERNOT · 2002 to 2006
$1.6M
Escape of Mycobacterium tuberculosis from the macrophage is regulated by eicosanoR56AI084161 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M, REMOLD, HEINZ GERNOT · 2009 to 2010
$1.1M
Antigen-specific CD8+ T cells and protective immunity to tuberculosisR56AI067731 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2012 to 2012
$507k
A Novel Mechanism of Innate Immunity Against TBR21AI050216 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI REMOLD, HEINZ GERNOT · 2001 to 2001
$336k
NIAID NIH HHS AI072143NIAID NIH HHS AI50216NIAID NIH HHS R01 AI047171NIAID NIH HHS R01 AI050216NIAID NIH HHS R01 AI067731NIAID NIH HHS R01 AI072143NIAID NIH HHS R01 AI47171NIAID NIH HHS R21 AI050216NIAID NIH HHS R56 AI084161
6 · The paper itself

Abstract

Eicosanoids regulate whether human and murine macrophages infected with Mycobacterium tuberculosis die by apoptosis or necrosis. The death modality is important since apoptosis is associated with diminished pathogen viability and should be viewed as a form of innate immunity. Apoptotic vesicles derived from infected macrophages are also an important source of bacterial antigens that can be acquired by dendritic cells to prime antigen-specific T cells. This review integrates in vitro and in vivo data on how apoptosis of infected macrophages is linked to development of T cell immunity against M. tuberculosis.

Indexed as

AnimalsApoptosisEicosanoidsHost-Pathogen InteractionsHumansImmunity, CellularMacrophagesMiceMycobacterium tuberculosisTuberculosisEicosanoids

Identifiers

PMID21458584
PMCPMC3130819

What OpenQuestion holds

Textmetadata
LicenceTDM
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.