Evidence map›Paper›PMID 22916020›Full record

ArticlePLoS pathogens2012

Listeria monocytogenes cytoplasmic entry induces fetal wastage by disrupting maternal Foxp3+ regulatory T cell-sustained fetal tolerance.

Jared H Rowe, James M Ertelt, Lijun Xin, Sing Sing Way

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-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

42 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Human Listeriosis.Clinical microbiology reviews · 2023
    Review
  11. A Framework for Understanding Maternal Immunity.Immunology and allergy clinics of North America · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. An Update Review on Listeria Infection in Pregnancy.Infection and drug resistance · 2021
    Review
  16. Review
  17. Review
  18. Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019
    Article
  19. Review
  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

4 authors at 2 institutions in 1 country.

Jared H RoweDepartment of Pediatrics and Microbiology, Center for Infectious Disease and Microbiology Translational Research, University of Minnesota School of Medicine, Minneapolis, Minnesota, United States of America.
James M Ertelt
Lijun Xin
Sing Sing Way
Stanford University · USUniversity of Minnesota · US

Funding

PATHOPHYSIOLOGY OF HUMAN BLOOD CELLST32HL007574 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Daniel Evan Bauer · 1985 to 2026
$18.4M
The Immune Pathogenesis of Prenatal Listeria monocytogenes InfectionR01AI100934 · NIAID · UNIVERSITY OF MINNESOTA · PI WAY, SING SING · 2012 to 2016
$2.3M
Regulatory T cells dictate immunity during persistent Salmonella infectionR01AI087830 · NIAID · UNIVERSITY OF MINNESOTA · PI WAY, SING SING · 2010 to 2014
$1.8M
Acute infection overrides PDL-1 mediated T cell suppression in autoimmune DMF30DK084674 · NIDDK · UNIVERSITY OF MINNESOTA · PI ROWE, JARED H. · 2009 to 2013
$208k
NHLBI NIH HHS T32 HL007574NIAID NIH HHS R01 AI087830NIAID NIH HHS R01AI087830NIAID NIH HHS R01 AI100934NIAID NIH HHS R01AI100934NIDDK NIH HHS F30 DK084674NIDDK NIH HHS F30DK084674
6 · The paper itself

Abstract

Although the intracellular bacterium Listeria monocytogenes has an established predilection for disseminated infection during pregnancy that often results in spontaneous abortion or stillbirth, the specific host-pathogen interaction that dictates these disastrous complications remain incompletely defined. Herein, we demonstrate systemic maternal Listeria infection during pregnancy fractures fetal tolerance and triggers fetal wastage in a dose-dependent fashion. Listeria was recovered from the majority of concepti after high-dose infection illustrating the potential for in utero invasion. Interestingly with reduced inocula, fetal wastage occurred without direct placental or fetal invasion, and instead paralleled reductions in maternal Foxp3(+) regulatory T cell suppressive potency with reciprocal expansion and activation of maternal fetal-specific effector T cells. Using mutants lacking virulence determinants required for in utero invasion, we establish Listeria cytoplasmic entry is essential for disrupting fetal tolerance that triggers maternal T cell-mediated fetal resorption. Thus, infection-induced reductions in maternal Foxp3(+) regulatory T cell suppression with ensuing disruptions in fetal tolerance play critical roles in pathogenesis of immune-mediated fetal wastage.

Indexed as

Forkhead Transcription FactorsImmune ToleranceAnimalsCytoplasmFemaleFetal ResorptionListeria monocytogenesListeriosisMiceMice, Inbred BALB CPregnancyPregnancy Complications, InfectiousT-Lymphocytes, RegulatoryForkhead Transcription FactorsFoxp3 protein, mouse

Identifiers

PMID22916020
PMCPMC3420962
OpenAlexW1971882398

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.