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Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
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Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
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Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines

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Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines
Journal Article

Interleukin 10 (IL-10)–Producing CD1dhiRegulatory B Cells From Schistosoma Haematobium–Infected Individuals Induce IL-10-Positive T Cells and Suppress Effector T-Cell Cytokines

2014
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Overview
Background. Chronic schistosome infections are associated with T-cell hyporesponsiveness and a strong regulatory network. Murine studies have shown that schistosome infections can induce regulatory CD1dhi B cells, which inhibit inflammatory responses. Here, we evaluated the influence of regulatory B cells (Bregs) on T-cell cytokines in vitro in human schistosomiasis. Methods. Gabonese young adults were recruited from areas where Schistosoma haematobium (S.h) infections were high or low endemic. The study participants were categorized as infected or uninfected from an high endemic area or uninfected from a low endemic (nonendemic) area. Their B cells were studied for Breg subset markers and cocultured with allogenic anti-CD3-stimulated CD4⁺ T cells, followed by T-cell cytokine analysis. Results. A greater percentage of B cells from S. haematobium-infected donors expressed cytoplasmic interleukin 10(IL-10) and membrane-bound latency-associated peptide/transforming growth factor β1, compared with uninfected donors. T cells produced less interferon γ, interleukin 4, and interleukin 17 upon coculture with B cells from schistosome-infected individuals only, while the conversion to CD25hiFoxP3⁻ and the percentage of IL-10⁺ T cells was enhanced. Interestingly, depletion of the prominent IL-10-producing B-cell subset, CD1dhi cells, resulted in less IL-10⁺ T cells in the S. haematobium-infected group, while levels of FoxP3⁻ regulatory T cells remained unaffected. Conclusions. Schistosomes can induce functional Bregs in humans that may be instrumental in general T-cell hyporesponsiveness and may contribute to the increased regulatory milieu found in schistosomiasis.