Plasmacytoid dendritic cells modulate nonprotective T-cell responses to genital infection by Chlamydia muridarum
Plasmacytoid dendritic cells modulate nonprotective T-cell responses to genital infection by Chlamydia muridarum
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DOI：
10.1111/j.1574-695x.2010.00653.x
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发表时间：
2010-04-01
影响因子：
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通讯作者：
Kelly, Kathleen A.
中科院分区：
文献类型：
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作者：
Moniz, Raymond J.;Chan, Ann M.;Kelly, Kathleen A.
鉴于其免疫调节能力，调节性T细胞（Treg）细胞可能在诱导对生殖器衣原体感染的保护性T细胞反应（Th1）中发挥重要作用。最近的研究表明，浆细胞样树突状细胞（pDC）对生殖器衣原体感染有反应，并且pDC可能是在这种感染中诱导Treg细胞的独特定位。在这里，我们提出的第一个数据表明，Treg流入引流淋巴结和生殖器衣原体感染的感染部位。我们发现，pDC耗竭改变了生殖道感染衣原体小鼠脾脏中Treg和非保护性炎症细胞[产生干扰素γ -(IFN γ)的CD8+ T和产生干扰素γ的自然杀伤T细胞]的数量。此外，pDC耗竭不会改变Th1细胞数量，表明pDC调节细胞可以抑制和促进生殖器衣原体感染期间的非保护性炎症。最后，我们证明了pDC的消耗导致感染消退后输卵管内不那么严重的扩张和胶原沉积，这表明pDC的活性与生殖道阴道C. muridarum感染后后遗症的形成有关。
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 [interferon gamma-(IFN gamma)-producing CD8+ T and IFN gamma-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.