Department of Pathology & Laboratory Medicine, Geffen School of Medicine, University of California, Los Angeles, CA 90095-1732, USA.
Am J Reprod Immunol. 2009 Jun;61(6):438-45. doi: 10.1111/j.1600-0897.2009.00704.x. Epub 2009 Apr 22.
Chlamydia trachomatis causes STI and reproductive dysfunction worldwide which is not preventable with antibiotics. Identifying a population of endocervical T cells to target in vaccine development would enhance efficacy.
Trafficking of murine CD4+ lymphocytes to Chlamydia muridarum infected genital tract (GT) tissue in vivo was measured using adoptive transfer studies of fluorescent CD4+ T cells from integrin β7-/- mice or mice which lack E-selectin on endothelial cells.
Murine in vivo migration studies showed that lack of α4β7 or E-selectin significantly reduced trafficking of CD4 T cells to the GT of mice infected with C. muridarum.
CD4+ T cells use at least two different adhesive mechanisms involving an integrin of the mucosal homing pathway and selectin pathway to accumulate in the GT during C. muridarum infection.
沙眼衣原体可导致性传播感染和生殖功能障碍,而抗生素对此无法预防。如果能识别出可作为疫苗开发靶点的宫颈内 T 细胞群,将能提高疫苗的效果。
通过将整合素β7-/- 小鼠或缺乏内皮细胞 E-选择素的小鼠的荧光 CD4+T 细胞过继转移至感染鼠型沙眼衣原体(Chlamydia muridarum)的生殖道组织,体内测量了鼠源 CD4+淋巴细胞向受染生殖道组织的转运情况。
体内迁移研究显示,缺乏 α4β7 或 E-选择素会显著减少 CD4 T 细胞向感染鼠型沙眼衣原体的小鼠生殖道的转运。
在鼠型沙眼衣原体感染期间,CD4+T 细胞至少使用两种不同的黏附机制,包括黏膜归巢途径的整合素和选择素途径,从而在生殖道内聚集。