Evidence map›Paper›PMID 24130498›Full record

ArticlePLoS pathogens2013

CXCR3-dependent CD4⁺ T cells are required to activate inflammatory monocytes for defense against intestinal infection.

Sara B Cohen, Kirk J Maurer, Charlotte E Egan, Steve Oghumu, Abhay R Satoskar, Eric Y Denkers

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.1field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Single cell analysisFrontiers in immunology · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. From Initiators to Effectors: Roadmap Through the Intestine During Encounter ofFrontiers in cellular and infection microbiology · 2020
    Review
  14. Key Limitations and New Insights Into theFrontiers in cellular and infection microbiology · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Sara B CohenDepartment of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, New York, United States of America.
Kirk J Maurer
Charlotte E Egan
Steve Oghumu
Abhay R Satoskar
Eric Y Denkers
Cornell University · USThe Ohio State University · US

Funding

Signal Transduction During Toxoplasma InfectionR01AI050617 · NIAID · CORNELL UNIVERSITY ITHACA · PI DENKERS, ERIC Y · 2002 to 2012
$3.3M
Role of intraepithelial T cells in Toxoplasma gondii-induced inflammatory ileitisR21AI083526 · NIAID · CORNELL UNIVERSITY · PI DENKERS, ERIC Y · 2009 to 2010
$422k
Visualization of CXCR3 allelic usage in vivoR03AI090231 · NIAID · OHIO STATE UNIVERSITY · PI SATOSKAR, ABHAY R · 2010 to 2011
$242k
NIAID NIH HHS AI090231NIAID NIH HHS AI50617NIAID NIH HHS AI83526NIAID NIH HHS R01 AI050617NIAID NIH HHS R03 AI090231NIAID NIH HHS R21 AI083526
6 · The paper itself

Abstract

Chemokines and their receptors play a critical role in orchestrating immunity to microbial pathogens, including the orally acquired Th1-inducing protozoan parasite Toxoplasma gondii. Chemokine receptor CXCR3 is associated with Th1 responses, and here we use bicistronic CXCR3-eGFP knock-in reporter mice to demonstrate upregulation of this chemokine receptor on CD4⁺ and CD8⁺ T lymphocytes during Toxoplasma infection. We show a critical role for CXCR3 in resistance to the parasite in the intestinal mucosa. Absence of the receptor in Cxcr3⁻/⁻ mice resulted in selective loss of ability to control T. gondii specifically in the lamina propria compartment. CD4⁺ T cells were impaired both in their recruitment to the intestinal lamina propria and in their ability to secrete IFN-γ upon stimulation. Local recruitment of CD11b⁺Ly6C/G⁺ inflammatory monocytes, recently reported to be major anti-Toxoplasma effectors in the intestine, was not impacted by loss of CXCR3. However, inflammatory monocyte activation status, as measured by dual production of TNF-α and IL-12, was severely impaired in Cxcr3⁻/⁻ mice. Strikingly, adoptive transfer of wild-type but not Ifnγ⁻/⁻ CD4⁺ T lymphocytes into Cxcr3⁻/⁻ animals prior to infection corrected the defect in inflammatory macrophage activation, simultaneously reversing the susceptibility phenotype of the knockout animals. Our results establish a central role for CXCR3 in coordinating innate and adaptive immunity, ensuring generation of Th1 effectors and their trafficking to the frontline of infection to program microbial killing by inflammatory monocytes.

Indexed as

Immunity, CellularImmunity, InnateAnimalsCD8-Positive T-LymphocytesInterferon-gammaIntestinal DiseasesMiceMice, KnockoutMonocytesReceptors, CXCR3Th1 CellsToxoplasmaToxoplasmosisCxcr3 protein, mouseInterferon-gammaReceptors, CXCR3

Identifiers

PMID24130498
PMCPMC3795032
OpenAlexW2061718713

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.