Evidence map›Paper›PMID 12438372›Full record

ArticleInfection and immunity2002

The function of gamma interferon-inducible GTP-binding protein IGTP in host resistance to Toxoplasma gondii is Stat1 dependent and requires expression in both hematopoietic and nonhematopoietic cellular compartments.

Carmen M Collazo, George S Yap, Sara Hieny, Patricia Caspar, Carl G Feng, Gregory A Taylor, Alan Sher

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.2field-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

44 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. The Activin Receptor, Activin-Like Kinase 4, MediatesFrontiers in cellular and infection microbiology · 2019
    Article
  7. Clinical microbiology reviews · 2017
    Review
  8. Article
  9. Article
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  11. Article
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  17. Article
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  20. Upregulation of interferon-gamma-induced genes during prion infection.Journal of toxicology and environmental health. Part A · 2011
    Article
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

7 authors at 4 institutions in 1 country.

Carmen M CollazoImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. CCOLLAZO@niaid.nih.gov
George S Yap
Sara Hieny
Patricia Caspar
Carl G Feng
Gregory A Taylor
Alan Sher
National Institute of Allergy and Infectious Diseases · USBrown University · USDuke University Hospital · USNational Institutes of Health · US

Funding

Immune Regulation In Toxoplasmosis And Other Opportunistic InfectionsZIAAI000579 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$7.8M
STUDIES ON IMMUNE REGULATION IN TOXOPLASMOSISZ01AI000579 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHER, ALAN · 1990 to 2008
$4.0M
6 · The paper itself

Abstract

IGTP is a member of the 47-kDa family of gamma interferon (IFN-gamma)-induced GTPases. We have previously shown that IGTP is critical for host resistance to Toxoplasma gondii infection. In the present study, we demonstrate that T. gondii-induced IGTP expression in vivo and IFN-gamma-driven synthesis of the protein in vitro are dependent on Stat1. Consistent with this observation, Stat1-deficient animals succumbed to T. gondii infection with the same rapid kinetics as IGTP(-/-) mice. To ascertain the cellular levels at which IGTP functions in host control of acute infection, we constructed reciprocal bone marrow chimeras between IGTP-deficient and wild-type mice. Resistance to infection was observed only when IGTP was present in both hematopoietic and nonhematopoietic compartments. To assess the possible contribution of IGTP to the maintenance of parasite latency, partial chemotherapy was used to allow the establishment of chronic infection in IGTP-deficient animals. Upon cessation of drug treatment, these animals showed delayed mortality compared with similarly infected and treated IFN-gamma-deficient or inducible nitric oxide synthase-deficient mice, which succumbed rapidly. Parallel experiments performed with drug-treated bone marrow chimeras supported a role for the hematopoietic compartment in this NO-dependent, IGTP-independent control of chronic infection. Taken together, our findings demonstrate that host resistance mediated by IGTP is a Stat1-induced function which in the case of T. gondii acts predominantly to restrict acute as opposed to chronic infection. This effector mechanism requires expression of IGTP in cells of both hematopoietic and nonhematopoietic origin. In contrast, in latent infection, hematopoietically derived cells mediate resistance by means of a largely NO-dependent pathway.

Indexed as

Acute DiseaseAnimalsBrainCellsChronic DiseaseDNA-Binding ProteinsGTP PhosphohydrolasesHematopoietic Stem CellsInterferon-gammaMiceMice, Inbred C57BLNitric OxideSTAT1 Transcription FactorToxoplasmaToxoplasmosis, AnimalTrans-ActivatorsDNA-Binding ProteinsGTP PhosphohydrolasesIgtp protein, mouseInterferon-gammaNitric OxideStat1 protein, mouseSTAT1 Transcription FactorTrans-Activators

Identifiers

PMID12438372
PMCPMC132942
OpenAlexW2152234597

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.