Identification of homing receptors that mediate the recruitment of CD4 T cells to the genital tract following intravaginal infection with Chlamydia trachomatis
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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DOI：
10.1128/iai.65.12.5198-5208.1997
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发表时间：
1997-12-01
影响因子：
3.1
通讯作者：
Rank, RG
中科院分区：
文献类型：
--
作者：
Kelly, KA;Rank, RG
小鼠生殖道感染沙眼衣原体（Chlamydia trachomatis，MoPn）引起的局部细胞免疫反应主要由Th 1 CD 4细胞介导。在沙眼衣原体感染的研究中，我们通过鉴定支持CD 4淋巴细胞迁移到生殖器粘膜的分子来研究介导该过程的机制。我发现，在原发性和攻击性MoPn感染期间，主要是CD 4细胞被募集到生殖道（GT）。初次接种后21天达到峰值水平（磅）（15.4% +/- 2.7%）和7天（31.3% +/-8.5%），但在感染消退后减少。CD 4细胞似乎响应感染而被募集到GT，因为这些细胞表达活化或记忆细胞的特征，我们还观察到在感染过程中GT CD 4细胞上含有LFA-1（CD 11 a）和α 4（CD 49 d）的归巢受体的上调。此外，在GT CD 4细胞上检测到粘膜归巢受体链β 7，而不是外周归巢受体链β 1（CD 29），MoPn感染的GT组织表达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）和粘膜血管地址素细胞粘附分子1（MAdCAM-1），其对应于GT CD 4细胞上的归巢受体。有趣的是，VCAM-1和MAdCAM-1在未感染小鼠的GT中不表达，但在感染后被暂时诱导，表明GT中内皮配体的表达受衣原体感染的调节。这些数据表明，CD 4细胞向GT的募集是通过LFA-1：ICAM-1和α 4 β 7：MAdCAM-1-VCAM-1相互作用介导的。
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. me found that primarily CD4 cells were recruited to the genital tract (GT) during primary and challenge MoPn infection. Peak levels were Pound 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 alpha 4 (CD49d) on GT CD4 cells over the course of infection. Furthermore, the mucosal homing receptor chain, beta 7, but not the peripheral homing receptor chain beta 1 (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 alpha 4 beta 7:MAdCAM-1-VCAM-1 interactions.