Evidence map›Paper›PMID 29762680›Full record

ReviewPathogens and disease2018

Tuberculosis and the art of macrophage manipulation.

S Upadhyay, E Mittal, J A Philips

Open access · bronzeAbstract readReview
In one paragraph

Review in Pathogens and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
8.3field-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

95 citing papers in PubMed, 178 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Sorting nexin 5 mediates antigen presentation and immunity againstbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Biotechnologia · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Journal of clinical tuberculosis and other mycobacterial diseases · 2024
    Review
  20. Article

35 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.

S UpadhyayDivision of Infectious Diseases, Department of Medicine, Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
E MittalDivision of Infectious Diseases, Department of Medicine, Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
J A PhilipsDivision of Infectious Diseases, Department of Medicine, Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Washington University in St. Louis · US

Funding

Mechanisms of Innate Immune Evasion by Mycobacterium TuberculosisR01AI130454 · NIAID · WASHINGTON UNIVERSITY · PI JENNIFER A PHILIPS · 2017 to 2026
$5.9M
THE ROLE OF ESCRT IN MACROPHAGE RESISTANCE TO MYCOBACTERIAR01AI087682 · NIAID · WASHINGTON UNIVERSITY · PI PHILIPS, JENNIFER A · 2011 to 2022
$4.9M
Targeting Fatty Acid Metabolism to Treat TBR21AI128427 · NIAID · WASHINGTON UNIVERSITY · PI PHILIPS, JENNIFER A · 2017 to 2018
$419k
NIAID NIH HHS R01 AI087682NIAID NIH HHS R01 AI130454NIAID NIH HHS R21 AI128427NIH HHS R01 AI087682NIH HHS R01 AI130454NIH HHS R21 AI128427
6 · The paper itself

Abstract

Macrophages are first-line responders against microbes. The success of Mycobacterium tuberculosis (Mtb) rests upon its ability to convert these antimicrobial cells into a permissive cellular niche. This is a remarkable accomplishment, as the antimicrobial arsenal of macrophages is extensive. Normally bacteria are delivered to an acidic, degradative lysosome through one of several trafficking pathways, including LC3-associated phagocytosis (LAP) and autophagy. Once phagocytozed, the bacilli are subjected to reactive oxygen and nitrogen species, and they induce the expression of proinflammatory cytokines, which serve to augment host responses. However, Mtb hijacks these host defense mechanisms, manipulating host cellular trafficking, innate immune responses, and cell death pathways to its benefit. The complex series of measures and countermeasures between host and pathogen ultimately determines the outcome of infection. In this review, we focus on the diverse effectors that Mtb uses in its multipronged effort to subvert the innate immune responses of macrophages. We highlight recent advances in understanding the molecular interface of the Mtb-macrophage interaction.

Indexed as

AutophagyGene Expression RegulationHost-Pathogen InteractionsHumansImmunity, InnateLysosomesMacrophagesMicrotubule-Associated ProteinsMycobacterium tuberculosisPhagocytosisSignal TransductionTuberculosisType VII Secretion SystemsMAP1LC3A protein, humanMicrotubule-Associated ProteinsType VII Secretion Systems

Identifiers

PMID29762680
PMCPMC6251593
OpenAlexW2797949377

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.