Plasmacytoid dendritic cells modulate nonprotective T-cell responses to genital infection by Chlamydia muridarum.

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Given their immune-modulating capacity, regulatory T cells (Treg) cells may be important players in the induction of the protective T-cell response (Th1) to genital chlamydial infection. Recent work has demonstrated that plasmacytoid dendritic cells (pDC) respond to genital chlamydial infection, and that pDC may be uniquely positioned for the induction of Treg cells during this infection. Here, we present the first data demonstrating that Treg influx into the draining lymph node and the site of infection during genital chlamydial infection. We found that pDC depletion altered the numbers of Treg and nonprotective inflammatory cells [interferongamma-(IFNgamma)-producing CD8+ T and IFNgamma-producing natural killer T cells] in the spleens of mice genitally infected with Chlamydia muridarum. Furthermore, pDC depletion did not alter Th1 cell numbers, indicating that pDC modulate cells that could inhibit and promote nonprotective inflammation during genital chlamydial infection. Finally, we demonstrate that depletion of pDC results in less severe dilation and collagen deposition in the oviduct following resolution of infection, implicating pDC activity in the formation of sequelae following genital C. muridarum infection.