Evidence map›Paper›PMID 22147768›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Microbial infection-induced expansion of effector T cells overcomes the suppressive effects of regulatory T cells via an IL-2 deprivation mechanism.

Alicia Benson, Sean Murray, Prashanthi Divakar, Nikolay Burnaevskiy, Reed Pifer, James Forman, Felix Yarovinsky

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

57 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IL-27 promotes Treg cell expression of CD122 and fitness at homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Developmentally distinct CD4Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Article
  12. Article
  13. Immunoregulatory Effects of Tolerogenic Probiotics in Multiple Sclerosis.Advances in experimental medicine and biology · 2021
    Review
  14. The Binary Classification of Protein Kinases.Journal of inflammation research · 2021
    Article
  15. Article
  16. Review
  17. From Initiators to Effectors: Roadmap Through the Intestine During Encounter ofFrontiers in cellular and infection microbiology · 2020
    Review
  18. Article
  19. Article
  20. Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019
    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 1 institution in 1 country.

Alicia BensonDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sean Murray
Prashanthi Divakar
Nikolay Burnaevskiy
Reed Pifer
James Forman
Felix Yarovinsky
The University of Texas Southwestern Medical Center · US

Funding

Cellular and molecular mechanisms of host resistance to Toxoplasma gondiiR01AI085263 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI YAROVINSKY, FELIX · 2010 to 2014
$1.9M
NIAID NIH HHS R01 AI085263
6 · The paper itself

Abstract

Foxp3(+) regulatory T (Treg) cells are a critical cell population that suppresses T cell activation in response to microbial and viral pathogens. We identify a cell-intrinsic mechanism by which effector CD4(+) T cells overcome the suppressive effects of Treg cells in the context of three distinct infections: Toxoplasma gondii, Listeria monocytogenes, and vaccinia virus. The acute responses to the parasitic, bacterial, and viral pathogens resulted in a transient reduction in frequency and absolute number of Treg cells. The infection-induced partial loss of Treg cells was essential for the initiation of potent Th1 responses and host protection against the pathogens. The observed disappearance of Treg cells was a result of insufficiency in IL-2 caused by the expansion of pathogen-specific CD4(+) T cells with a limited capacity of IL-2 production. Exogenous IL-2 treatment during the parasitic, bacterial, and viral infections completely prevented the loss of Treg cells, but restoration of Treg cells resulted in a greatly enhanced susceptibility to the pathogens. These results demonstrate that the transient reduction in Treg cells induced by pathogens via IL-2 deprivation is essential for optimal T cell responses and host resistance to microbial and viral pathogens.

Indexed as

Acute DiseaseAnimalsCD4 Lymphocyte CountDisease ResistanceEpitopes, T-LymphocyteInterleukin-2ListeriosisLymphocyte ActivationLymphopeniaMiceMice, Inbred C57BLMice, TransgenicTh1 CellsT-Lymphocytes, RegulatoryToxoplasmosis, AnimalVacciniaEpitopes, T-LymphocyteInterleukin-2

Identifiers

PMID22147768
PMCPMC3253229
OpenAlexW2100457521

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.