Evidence map›Paper›PMID 18806793›Full record

ArticleNature immunology2008

The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-gamma-induced cell death.

Carl G Feng, Lixin Zheng, Dragana Jankovic, André Báfica, Jennifer L Cannons, Wendy T Watford, Damien Chaussabel, Sara Hieny, Patricia Caspar, Pamela L Schwartzberg and 2 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Novel Targets for the Development of Tuberculosis Vaccine.Current drug discovery technologies · 2025
    Review
  5. Article
  6. Type I IFN signaling in the absence of IRGM1 promotesbioRxiv : the preprint server for biology · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Host Autophagy DuringFrontiers in microbiology · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 1 country.

Carl G FengLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. cfeng@niaid.nih.gov
Lixin Zheng
Dragana Jankovic
André Báfica
Jennifer L Cannons
Wendy T Watford
Damien Chaussabel
Sara Hieny
Patricia Caspar
Pamela L Schwartzberg
Michael J Lenardo
Alan Sher
Division of Parasitic Diseases and Malaria · USNational Human Genome Research Institute · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · USBaylor University · US

Funding

Genetic and Biochemical Approaches to Tyrosine Kinase FunctionZIAHG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 2009 to 2018
$20.8M
Molecular Mechanisms and Treatment Of Autoimmunity In Man And Animal ModelsZIAAI000717 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, HELEN CHUN-HUI · 2009 to 2025
$13.2M
Regulation Of Immunopathology In Bacterial And Parasitic DiseaseZIAAI000843 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$11.1M
Regulation Of Immunopathology In Bacterial And Parasitic DiseaseZ01AI000843 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHER, ALAN · 1999 to 2008
$4.1M
STUDIES ON IMMUNE REGULATION IN TOXOPLASMOSISZ01AI000579 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHER, ALAN · 1990 to 2008
$4.0M
Innate Determinants of Microbial ImmunityZ01AI001044 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2008 to 2008
$648k
Intramural NIH HHS Z01 AI000579Intramural NIH HHS Z01 AI000843
6 · The paper itself

Abstract

Mice deficient in the interferon-gamma (IFN-gamma)-inducible, immunity-related GTPase Irgm1 have defective host resistance to a variety of intracellular pathogens. This greater susceptibility to infection is associated with impaired IFN-gamma-dependent macrophage microbicidal activity in vitro. Here we show that Irgm1 also regulated the survival of mature effector CD4(+) T lymphocytes by protecting them from IFN-gamma-induced autophagic cell death. Mice deficient in both IFN-gamma and Irgm1 were 'rescued' from the lymphocyte depletion and greater mortality that occurs in mice singly deficient in Irgm1 after mycobacterial infection. Our studies identify a feedback mechanism in the T helper type 1 response that limits the detrimental effects of IFN-gamma on effector T lymphocyte survival while promoting the antimicrobial functions of IFN-gamma.

Indexed as

AutophagyAnimalsCD4-Positive T-LymphocytesCell ProliferationCells, CulturedCell SurvivalFemaleGTP-Binding ProteinsInterferon-gammaLymphocyte ActivationMaleMiceMice, Inbred C57BLMice, KnockoutMycobacterium aviumReceptors, Antigen, T-CellGTP-Binding ProteinsIfi1 protein, mouseInterferon-gammaReceptors, Antigen, T-Cell

Identifiers

PMID18806793
PMCPMC2580721
OpenAlexW2074917064

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.