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首页> 外文期刊>Infection and immunity >Identification of homing receptors that mediate the recruitment of CD4 T cells to the genital tract following intravaginal infection with Chlamydia trachomatis.
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Identification of homing receptors that mediate the recruitment of CD4 T cells to the genital tract following intravaginal infection with Chlamydia trachomatis.

机译：在沙眼衣原体阴道内感染后介导CD4 T细胞募集到生殖道的归巢受体的鉴定。

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Murine genital infection induced with the mouse pneumonitis biovar of Chlamydia trachomatis (MoPn) elicits a short-lived protective immunity mediated primarily by Th1 CD4 cells. To understand the development of local cell-mediated immunity against C. trachomatis infection, we investigated the mechanism(s) which mediates CD4 lymphocyte migration to the genital mucosa by identifying molecules that could support this process. We found that primarily CD4 cells were recruited to the genital tract (GT) during primary and challenge MoPn infection. Peak levels were found 21 days after primary inoculation (15.4% +/- 2.7%) and 7 days (31.3% +/- 8.5%) after challenge but diminished after resolution of infection. The CD4 cells appeared to be recruited to the GT in response to infection since these cells expressed the profile of activated, or memory, cells. We also observed up-regulation of homing receptors containing LFA-1 (CD11a) and alpha4 (CD49d) on GT CD4 cells over the course of infection. Furthermore, the mucosal homing receptor chain, beta7, but not the peripheral homing receptor chain beta1 (CD29), was detected on GT CD4 cells. MoPn-infected GT tissue expressed the endothelial cell ligands vascular cell adhesion molecule 1 (VCAM-1), intracellular adhesion molecule 1 (ICAM-1), and mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1), which correspond to the homing receptors on GT CD4 cells. Interestingly, VCAM-1 and MAdCAM-1 were not expressed in the GTs of uninfected mice but were temporarily induced following infection, indicating that expression of endothelial ligands in the GT are regulated by chlamydial infection. These data suggest that recruitment of CD4 cells to the GT is mediated through LFA-1:ICAM-1 and alpha4beta7:MAdCAM-1-VCAM-1 interactions.
机译：沙眼衣原体（MoPn）小鼠肺炎病毒引起的鼠生殖器感染引起了主要由Th1 CD4细胞介导的短暂保护性免疫。为了了解针对沙眼衣原体感染的局部细胞介导的免疫反应的发展，我们通过鉴定可以支持该过程的分子，研究了介导CD4淋巴细胞迁移至生殖器粘膜的机制。我们发现在原发性和挑战性MoPn感染期间，主要是CD4细胞被募集到生殖道（GT）。在初次接种后21天（15.4％+/- 2.7％）和攻击后7天（31.3％+/- 8.5％）发现峰值水平，但在感染消退后消失。由于这些细胞表达了活化或记忆细胞的特征，因此似乎对CD4细胞有新的反应。我们还观察到在感染过程中，GT CD4细胞上的包含LFA-1（CD11a）和alpha4（CD49d）的归巢受体上调。此外，在GT CD4细胞上检测到粘膜归巢受体链β7，但未检测到外周归巢受体链β1（CD29）。 MoPn感染的GT组织表达了内皮细胞配体血管细胞粘附分子1（VCAM-1），细胞内粘附分子1（ICAM-1）和粘膜血管地址在细胞粘附分子1（MAdCAM-1）中，这与归巢相对应GT CD4细胞上的受体。有趣的是，VCAM-1和MAdCAM-1在未感染小鼠的GT中未表达，但在感染后被暂时诱导，这表明衣原体感染可调节GT中的内皮配体表达。这些数据表明CD4细胞募集到GT是通过LFA-1：ICAM-1和alpha4beta7：MAdCAM-1-VCAM-1相互作用介导的。

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