CXCR3 and CCR5 are both required for T cell-mediated protection against C. trachomatis infection in the murine genital mucosa.
CXCR3 and CCR5 are both required for T cell-mediated protection against C. trachomatis infection in the murine genital mucosa.
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趋化因子受体通过协调的趋化因子梯度将 T 淋巴细胞引导至感染部位，从而将其募集至特定组织。尽管已经阐明了归巢到某些粘膜部位（例如皮肤和肠道）所需的受体的鉴定，但将淋巴细胞引导至生殖器粘膜的受体仍然相对未知。在这里，我们确定趋化因子受体 CXCR3 和 CCR5 对于沙眼衣原体感染期间 T 淋巴细胞进入生殖道至关重要。缺乏 CXCR3 或 CCR5 的衣原体特异性 CD4+ 转基因 T 细胞在感染后不会在生殖器粘膜中积聚。 CXCR3 或 CCR5 的缺失会损害衣原体特异性 T 细胞的保护能力，而缺乏这两种受体的 T 细胞则完全没有保护能力。这些结果表明CXCR3和CCR5是主要的趋化因子受体，它们在衣原体感染期间协同作用促进归巢到生殖器粘膜。
Chemokine receptors direct T lymphocytes to the site of an infection by following coordinated chemokine gradients, which allow their recruitment to specific tissues. Although identification of receptors needed for homing to some mucosal sites, such as skin and gut, have been elucidated, the receptors that direct lymphocytes to the genital mucosa remain relatively uncharacterized. Here we identify that the chemokine receptors CXCR3 and CCR5 are pivotal for T lymphocyte access to the genital tract during Chlamydia trachomatis infection. Chlamydia specific CD4+ transgenic T cells that lack CXCR3 or CCR5 do not accumulate in the genital mucosa following infection. Loss of either CXCR3 or CCR5 impairs the protective capacity of Chlamydia specific T cells, while T cells lacking both receptors are completely non-protective. These results show that CXCR3 and CCR5 are the predominant chemokine receptors, which act cooperatively to promote homing to the genital mucosa during Chlamydia infection.
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影响因子：
64.8
作者：
通讯作者：
--
影响因子：
30.5
作者：
通讯作者：
--
影响因子：
5.4
作者：
Fadell, Shaza A.;Bromley, Shannon K.;Medoff, Benjamin D.;Luster, Andrew D.
通讯作者：
Luster, Andrew D.
影响因子：
4.4
作者：
de Lemos, C;Christensen, JE;Thomsen, AR
通讯作者：
Thomsen, AR
DOI：
10.1084/jem.184.6.2433
发表时间：
1996-12-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Granelli-Piperno A;Moser B;Pope M;Chen D;Wei Y;Isdell F;O'Doherty U;Paxton W;Koup R;Mojsov S;Bhardwaj N;Clark-Lewis I;Baggiolini M;Steinman RM
通讯作者：
Steinman RM