Moniz Raymond J, Chan Ann M, Gordon Lynn K, Braun Jonathan, Arditi Moshe, Kelly Kathleen A
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA, USA.
FEMS Immunol Med Microbiol. 2010 Apr;58(3):397-404. doi: 10.1111/j.1574-695X.2010.00653.x. Epub 2010 Jan 19.
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.
鉴于其免疫调节能力，调节性T细胞（Treg）可能是诱导针对生殖道衣原体感染的保护性T细胞应答（Th1）的重要参与者。最近的研究表明，浆细胞样树突状细胞（pDC）对生殖道衣原体感染有反应，并且在这种感染期间，pDC可能在诱导Treg细胞方面具有独特的地位。在此，我们首次展示了在生殖道衣原体感染期间Treg流入引流淋巴结和感染部位的数据。我们发现，在经鼠衣原体生殖道感染的小鼠脾脏中，pDC耗竭改变了Treg和非保护性炎性细胞[产生干扰素γ（IFNγ）的CD8 + T细胞和产生IFNγ的自然杀伤T细胞]的数量。此外，pDC耗竭并未改变Th1细胞数量，这表明pDC调节的细胞在生殖道衣原体感染期间可抑制和促进非保护性炎症。最后，我们证明，pDC耗竭导致感染消退后输卵管中扩张和胶原沉积减轻，这表明pDC活性与鼠衣原体生殖道感染后后遗症的形成有关。
