Evidence map›Paper›PMID 25319335›Full record

ReviewImmunological reviews2014

Beyond macrophages: the diversity of mononuclear cells in tuberculosis.

Smita Srivastava, Joel D Ernst, Ludovic Desvignes

Abstract readReview
In one paragraph

Review in Immunological reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 172 citations in OpenAlex.

  1. Trial
  2. Article
  3. HowVaccines · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Single-cell analysis revealsScience advances · 2025
    Article
  14. The Role of PGE2 in Age-related Diseases.Current drug targets · 2025
    Review
  15. Article
  16. The frequency of CD38Nature communications · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

54 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

3 authors at 1 institution in 1 country.

Smita SrivastavaDepartments of Medicine, Microbiology, and Pathology, New York University School of Medicine, New York, NY, USA.
Joel D Ernst
Ludovic Desvignes
New York University · US

Funding

Initiation of the Immune Response to M. tuberculosisR01AI051242 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ERNST, JOEL D. · 2002 to 2019
$8.3M
Mycobacterium tuberculosis evasion of CD4+ T cells in vivoR01AI084041 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ERNST, JOEL D. · 2010 to 2015
$2.3M
Mycobacterium tuberculosis evasion of CD4+ T cells in vivoR56AI084041 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ERNST, JOEL D. · 2009 to 2009
$317k
NIAID NIH HHS AI051242NIAID NIH HHS AI084041NIAID NIH HHS R01 AI051242NIAID NIH HHS R01 AI084041NIAID NIH HHS R56 AI084041
6 · The paper itself

Abstract

Mycobacterium tuberculosis, the bacterium that causes tuberculosis (TB), is an intracellular pathogen of mononuclear phagocytes. Although M. tuberculosis has traditionally been thought to survive and replicate in macrophages, recent work in our laboratory and others has revealed that M. tuberculosis infects multiple subsets of mononuclear phagocytes in vivo and in vitro. In experimental animals, M. tuberculosis infects no fewer than five distinct cell subsets in the lungs, including resident alveolar macrophages and 4 types of cells that recruited to the lungs in response to inflammatory signals: neutrophils, monocytes, interstitial macrophages, and dendritic cells. A characteristic of the adaptive immune response in TB is that it is delayed for several weeks following infection, and we have determined that this delay is due to prolonged residence of the bacteria in lung phagocytes prior to acquisition of the bacteria by dendritic cells. Among the mechanisms used by M. tuberculosis to delay acquisition by dendritic cells is to inhibit apoptosis of alveolar macrophages and neutrophils, which sequester the bacteria and prevent their acquisition by dendritic cells in the early stages of infection. We hypothesize that each infected cell subset makes a distinct contribution to the overall biology of M. tuberculosis and allows the bacteria to evade elimination by T-cell responses and to avoid rapid killing by antimycobacterial drugs.

Indexed as

Adaptive ImmunityAnimalsCell DifferentiationCell MovementDendritic CellsHumansImmunity, InnateMacrophagesMacrophages, AlveolarMononuclear Phagocyte SystemNeutrophilsPhenotypeTuberculosisantigen presentationcytokinedendritic cellmacrophagemonocytetuberculosis

Identifiers

PMID25319335
PMCPMC4203409
OpenAlexW2067579914

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.