Evidence map›Paper›PMID 22354319›Full record

ArticleMucosal immunology2012

Neisseria gonorrhoeae selectively suppresses the development of Th1 and Th2 cells, and enhances Th17 cell responses, through TGF-β-dependent mechanisms.

Y Liu, E A Islam, G A Jarvis, S D Gray-Owen, M W Russell

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Article
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  4. Inhibition ofmBio · 2026
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  7. Frontiers in microbiology · 2026
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  8. Review
  9. The interplay betweenInfection and immunity · 2025
    Article
  10. Influence of cervicovaginal microbiota onMicrobial cell (Graz, Austria) · 2025
    Review
  11. Protection againstFrontiers in immunology · 2025
    Article
  12. Editorial: Reviews in microbial pathogenesis.Frontiers in microbiology · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  18. Clinical microbiology reviews · 2024
    Review
  19. Article
  20. Article

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

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

5 authors at 3 institutions in 2 countries.

Y LiuDepartment of Microbiology and Immunology, University at Buffalo, Buffalo, New York, USA. yingruli@buffalo.edu
E A Islam
G A Jarvis
S D Gray-Owen
M W Russell
University at Buffalo, State University of New York · USUniversity of Toronto · CAUniversity of California, San Francisco · US

Funding

Bacterial STI and Innate Immunity in HIV SusceptibilityR01AI063927 · NIAID · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI JARVIS, GARY A · 2005 to 2009
$2.9M
Gonococcal Inflammatory Immune ResponsesR21AI074791 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI RUSSELL, MICHAEL W · 2009 to 2010
$434k
CIHR MOP-15499NIAID NIH HHS AI063927NIAID NIH HHS R01 AI063927NIAID NIH HHS R21 AI074791
6 · The paper itself

Abstract

Infection with Neisseria gonorrhoeae does not induce specific immunity or immune memory. Our previous studies in a murine model of vaginal gonococcal infection showed that innate immunity governed by Th17 cells was a critical aspect of the immune response elicited by this pathogen. Herein we show that N. gonorrhoeae selectively inhibited Th1 and Th2 cells and enhanced Th17 cell development through the induction of TGF-β. Whereas Th17 responses depended on gonococcal lipooligosaccharide acting through TLR4, the inhibitory effect of N. gonorrhoeae on Th1/Th2 responses involved gonococcal Opa proteins. In vitro Th17 responses to N. gonorrhoeae could be diverted to Th1/Th2 by blockade of TGF-β, but not by blockade of IL-17. The results reveal that N. gonorrhoeae suppresses Th1/Th2-mediated adaptive immune response through mechanisms dependent on TGF-β, and that this effect can be manipulated to promote the development of adaptive immunity.

Indexed as

Adaptive ImmunityAnimalsCells, CulturedDisease Models, AnimalGonorrheaHumansImmune EvasionImmunity, InnateImmunologic MemoryImmunomodulationMiceMice, Inbred StrainsMice, KnockoutNeisseria gonorrhoeaeTh17 CellsTh1 CellsTransforming Growth Factor beta

Identifiers

PMID22354319
PMCPMC3328619
OpenAlexW1969606058

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.