Evidence map›Paper›PMID 22980326›Full record

ArticleCell host & microbe2012

Efferocytosis is an innate antibacterial mechanism.

Constance J Martin, Matthew G Booty, Tracy R Rosebrock, Cláudio Nunes-Alves, Danielle M Desjardins, Iris Keren, Sarah M Fortune, Heinz G Remold, Samuel M Behar

Abstract read
In one paragraph

Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.

0numbers the graph read from it
0cells of the map it votes in
172citing 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

172 citing papers in PubMed.

  1. Review
  2. Human memory CD4bioRxiv : the preprint server for biology · 2026
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. c-Myc inhibits macrophage antimycobacterial response inbioRxiv : the preprint server for biology · 2025
    Article
  16. Article
  17. Zinc-limitedInfection and immunity · 2025
    Article
  18. Building Spatiotemporal Understanding ofACS infectious diseases · 2025
    Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Constance J MartinDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Matthew G Booty
Tracy R Rosebrock
Cláudio Nunes-Alves
Danielle M Desjardins
Iris Keren
Sarah M Fortune
Heinz G Remold
Samuel M Behar

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
SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
Multidisciplinary HIV Training ProgramT32AI007387 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Daniel R. Kuritzkes · 1990 to 2026
$8.8M
Variation in M. tuberculosis in response to host selectionDP2OD001378 · OD · HARVARD SCHOOL OF PUBLIC HEALTH · PI FORTUNE, SARAH · 2007 to 2009
$2.5M
Apoptosis and efferocytosis: regulators of immunity to tuberculosisR01AI098637 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BEHAR, SAMUEL M · 2012 to 2016
$2.4M
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
South Carolina Clinical & Translational Research Institute (SCTR)TL1RR029881 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$1.1M
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
NCCDPHP CDC HHS DP2-0D001378NCRR NIH HHS TL1 RR029881NCRR NIH HHS UL1 RR029882NIAID NIH HHS 5P30AI060354NIAID NIH HHS P30 AI060354NIAID NIH HHS R01 AI072143NIAID NIH HHS R01AI072143NIAID NIH HHS R01 AI098637NIAID NIH HHS R56 AI084161NIAID NIH HHS R56AI084161NIAID NIH HHS T32 AI007387NIAID NIH HHS T32-AI07387
6 · The paper itself

Abstract

Mycobacterium tuberculosis persists within macrophages in an arrested phagosome and depends upon necrosis to elude immunity and disseminate. Although apoptosis of M. tuberculosis-infected macrophages is associated with reduced bacterial growth, the bacteria are relatively resistant to other forms of death, leaving the mechanism underlying this observation unresolved. We find that after apoptosis, M. tuberculosis-infected macrophages are rapidly taken up by uninfected macrophages through efferocytosis, a dedicated apoptotic cell engulfment process. Efferocytosis of M. tuberculosis sequestered within an apoptotic macrophage further compartmentalizes the bacterium and delivers it along with the apoptotic cell debris to the lysosomal compartment. M. tuberculosis is killed only after efferocytosis, indicating that apoptosis itself is not intrinsically bactericidal but requires subsequent phagocytic uptake and lysosomal fusion of the apoptotic body harboring the bacterium. While efferocytosis is recognized as a constitutive housekeeping function of macrophages, these data indicate that it can also function as an antimicrobial effector mechanism.

Indexed as

ApoptosisPhagocytosisAnimalsCells, CulturedImmune EvasionLysosomesMacrophagesMiceMice, Inbred C57BLMicrobial ViabilityMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMycobacterium tuberculosis

Identifiers

PMID22980326
PMCPMC3517204

What OpenQuestion holds

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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.