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 Janowicz, Kate R. Fortney, Barry Katz, Stanley Spinola

Research output: Contribution to journalArticle

11 Citations (Scopus)

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 (Treg) 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+, CD127lo/-, 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 γ, 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. ducreyireactive CD4+ T cells. Our results indicate that the population of CD4 +CD25+CD127lo/-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.

Original languageEnglish
Pages (from-to)1839-1848
Number of pages10
JournalJournal of Infectious Diseases
Volume201
Issue number12
DOIs
StatePublished - Jun 15 2010

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Haemophilus ducreyi
Regulatory T-Lymphocytes
Volunteers
T-Lymphocytes
Infection
Chancroid
Interferons
Ulcer
Bacteria

ASJC Scopus subject areas

  • Infectious Diseases
  • Immunology and Allergy
  • Medicine(all)

Cite this

Role played by CD4+FOXP3+ regulatory T cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteers. / Li, Wei; Tenner-Racz, Klara; Racz, Paul; Janowicz, Diane; Fortney, Kate R.; Katz, Barry; Spinola, Stanley.

In: Journal of Infectious Diseases, Vol. 201, No. 12, 15.06.2010, p. 1839-1848.

Research output: Contribution to journalArticle

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