Evidence map›Paper›PMID 20443736›Full record

ArticleThe Journal of infectious diseases2010

Role played by CD4+FOXP3+ regulatory T Cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteers.

Wei Li, Klara Tenner-Racz, Paul Racz, Diane M Janowicz, Kate R Fortney, Barry P Katz, Stanley M Spinola

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Molecular pathogenesis ofMicrobiology and molecular biology reviews : MMBR · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Regulatory T cells in infection.Advances in immunology · 2011
    Review
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 2 institutions in 2 countries.

Wei LiDepartment of Medicine, Laboratory Medicine, Indiana University School of Medicine, Indianapolis, USA. wl1@iupui.edu
Klara Tenner-Racz
Paul Racz
Diane M Janowicz
Kate R Fortney
Barry P Katz
Stanley M Spinola
Indiana University School of MedicineBernhard Nocht Institute for Tropical Medicine · DE

Funding

INDIANA CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE (UL1): BPCAUL1RR025761 · NCRR · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2008 to 2011
$21.0M
VIRAL DETERMINANTS OF HSV DISEASE IN MICEU19AI031494 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SPINOLA, STANLEY M. · 1995 to 2009
$13.6M
PATHOGENESIS OF HAEMOPHILUS DUCREYI INFECTIONSR01AI027863 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SPINOLA, STANLEY M. · 1995 to 2013
$3.8M
Human Immune Response to Haemophilus Ducreyi InfectionR01AI059384 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SPINOLA, STANLEY M. · 2007 to 2011
$1.8M
PATHOGENESIS OF HAEMOPHILUS DUCREYI INFECTIONSR29AI027863 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SPINOLA, STANLEY M · 1990 to 1994
–
VARIABILITY IN HERPES SIMPLEX VIRUS GLYCOPROTEINS AND INFECTIVITYU01AI031494 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BYRNE, GERALD I · 1991 to 1994
–
NCRR NIH HHS UL1 RR025761NCRR NIH HHS UL RR025761NIAID NIH HHS AI059384NIAID NIH HHS AI27863NIAID NIH HHS AI31494NIAID NIH HHS R01 AI027863NIAID NIH HHS R01 AI059384NIAID NIH HHS U19 AI031494
6 · The paper itself

Abstract

Haemophilus ducreyi causes chancroid, a genital ulcer disease. Among human volunteers, the majority of experimentally infected individuals fail to clear the infection and form pustules. Here, we investigated the role played by CD4(+)FOXP3(+) regulatory T (T(reg)) cells in the formation of pustules. In pustules, there was a significant enrichment of CD4(+)FOXP3(+) T cells, compared with that in peripheral blood. The majority of lesional FOXP3(+) T cells were CD4(+), CD25(+), CD127(lo/-), and CTLA-4(+). FOXP3(+) T cells were found throughout pustules but were most abundant at their base. Significantly fewer lesional CD4(+)FOXP3(+) T cells expressed interferon gamma, compared with lesional CD4(+)FOXP3(-) effector T cells. Depletion of CD4(+)CD25(+) T cells from the peripheral blood of infected and uninfected volunteers significantly enhanced proliferation of H. ducreyi-reactive CD4(+) T cells. Our results indicate that the population of CD4(+)CD25(+)CD127(lo/-)FOXP3(+) T(reg) cells are expanded at H. ducreyi-infected sites and that these cells may play a role in suppressing the host immune response to the bacterium.

Indexed as

Immune ToleranceAdultCD4-Positive T-LymphocytesForkhead Transcription FactorsHaemophilus ducreyiHaemophilus InfectionsHuman ExperimentationHumansInterferon-gammaLymphocyte DepletionMaleSkin Diseases, BacterialT-Lymphocytes, RegulatoryYoung AdultForkhead Transcription FactorsFOXP3 protein, humanInterferon-gamma

Identifiers

PMID20443736
PMCPMC2873097
OpenAlexW2015201783

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.