Evidence map›Paper›PMID 28799902›Full record

ReviewCell host & microbe2017

Innate Immunity to Intracellular Pathogens: Balancing Microbial Elimination and Inflammation.

Gabriel Mitchell, Ralph R Isberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
9.5field-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

65 citing papers in PubMed, 121 citations in OpenAlex.

  1. Review
  2. Review
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  4. Review
  5. ENKD1 attenuates antibacterial immunity by facilitating TRIM21-mediated RUBCN degradation to suppress LC3-associated phagocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Phosphatidic acid production on the vacuole harboringProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
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  9. Article
  10. Article
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  13. The mitochondrial carboxylase PCCA interacts withApplied and environmental microbiology · 2024
    Article
  14. A Systemic Review on Fitness and Survival ofIndian journal of microbiology · 2024
    Review
  15. Article
  16. Frontiers in cellular and infection microbiology · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

5 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

2 authors at 2 institutions in 1 country.

Gabriel MitchellDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Ralph R IsbergDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, 150 Harrison Ave., Boston, MA 02111, USA. Electronic address: ralph.isberg@tufts.edu.
Tufts University · USUniversity of California, Berkeley · US

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI PORTNOY, DANIEL A · 2004 to 2025
$45.5M
Listeria Hemolysis and Escape From a VacuoleR01AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DANIEL A PORTNOY · 1993 to 2026
$10.1M
Control of Endoplasmic Reticulum Tubule Formation by Legionella pneumophilaR01AI113211 · NIAID · TUFTS UNIVERSITY BOSTON · PI ISBERG, RALPH R. · 2014 to 2018
$2.7M
Mammalian cell collaboration with bacterial type III secretionR01AI110684 · NIAID · TUFTS UNIVERSITY BOSTON · PI ISBERG, RALPH R. · 2016 to 2020
$2.1M
Howard Hughes Medical InstituteNIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI027655NIAID NIH HHS R01 AI110684NIAID NIH HHS R01 AI113211
6 · The paper itself

Abstract

Recent excitement regarding immune clearance of intracellular microorganisms has focused on two systems that maintain cellular homeostasis. One system includes cellular autophagy components that mediate degradation of pathogens in membrane-bound compartments, in a process termed xenophagy. The second system is driven by interferon-regulated GTPases that promote rupture of pathogen-containing vacuoles and microbial degradation. In the case of xenophagy, pathogen sequestration and compartmentalization suppress inflammation. In contrast, interferon-driven events can lead to exposure of pathogen-associated molecular patterns to the host cytosol with consequent inflammasome activation. Paradoxically, signals and factors involved in xenophagy also mobilize interferon-regulated GTPases, which drive the inflammatory response, indicating considerable cross-talk between these pathways. How these responses are prioritized remains to be understood. In this review, we describe mechanisms of intracellular pathogen clearance that rely on the autophagy machinery and interferon-regulated GTPases, and speculate how these pathways engage each other to balance pathogen elimination with inflammation.

Indexed as

Immunity, InnateAnimalsAutophagyCytoplasmGTP PhosphohydrolasesHost-Parasite InteractionsHumansInflammasomesInflammationInterferon-gammaInterferonsVacuolesGTP PhosphohydrolasesInflammasomesInterferon-gammaInterferonsautophagyGBPguanylate binding proteinsimmunity-regulated GTPasesinflammasomeinterferonIRGxenophagy

Identifiers

PMID28799902
PMCPMC5562164
OpenAlexW2744171534

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.