Abstract
Abstract CD4+FoxP3+CD25+ regulatory T cells (Tregs) have been shown to promote de novo Th17 differentiation and to themselves convert into IL-17-producing cells in certain inflammatory settings. However, whether Tregs can potentiate IL-17/Th17 responses to intracellular bacterial infection has not been established. Using a murine model of Chlamydia, we found that Tregs produced IL-17 upon Chlamydia infection and promoted IL-17 production by conventional CD4+ T cells in vitro. Correspondingly, in vivo depletion of Tregs by anti-CD25 antibody dramatically reduced the induction of IL-17-producing CD4+ T cells during Chlamydia genital tract infection. Consistent with reduced IL-17 responses, Treg-depleted mice displayed striking amelioration of neutrophil infiltration and pathology in genital tract tissue relative to control mice, despite comparable bacterial burden throughout the course of infection. Collectively, our data demonstrate an important role for Tregs in promoting IL-17/Th17 responses during intracellular bacterial infection.
Published Version
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