Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 201, Issue 12, Pages 1839-1848Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/652781
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Funding
- National Institute of Allergy and Infectious Diseases [AI27863, AI31494, AI059384]
- Competence Network for HIV/AIDS [FKZ 01KI0501]
- Indiana Clinical and Translational Sciences Institute [UL RR025761]
- German Ministry of Education and Research
- Indiana Clinical Research Center
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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.
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