Expression of CD1d and ligand-induced cytokine production are tissue specific in mucosal epithelia of the human lower reproductive tract
Expression of CD1d and ligand-induced cytokine production are tissue specific in mucosal epithelia of the human lower reproductive tract
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DOI：
10.1128/iai.01672-07
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发表时间：
2008-07-01
影响因子：
3.1
通讯作者：
Schust, Danny J.
中科院分区：
文献类型：
--
作者：
Kawana, Kei;Matsumoto, Junko;Schust, Danny J.
人类下生殖道（阴道、子宫颈和阴茎尿道）的粘膜上皮暴露于性传播微生物，包括沙眼衣原体。每种组织类型对沙眼衣原体感染的体内敏感性是非常不同的。 CD1d 在抗原呈递细胞（包括粘膜上皮细胞）的表面表达，并与不变的 NKT 细胞特异性相互作用。不变的 NKT 细胞在针对微生物的先天性和适应性免疫反应中发挥着重要作用。在这里，我们通过免疫组织化学评估了正常生殖组织中的 CD1d 表达。检查来自人类下生殖道（阴道、宫颈内膜和阴茎尿道）的永生化上皮细胞系的 CD1d 表达以及由 CD1d 交联诱导的配体诱导的细胞因子产生。正常组织中CD1d的表达在阴道中较强，但在子宫颈内膜和阴茎尿道中较弱。 γ 干扰素暴露在所有研究的细胞类型中诱导 CD1d 转录，其中阴道细胞的诱导最强。流式细胞术显示阴道和阴茎尿道上皮细胞中 CD1d 的细胞表面表达，但宫颈内膜细胞中不表达。通过单克隆抗体交联连接表面表达的 CD1d 促进了阴道和阴茎尿道细胞中白细胞介素 12 (IL-12) 和 IL-15 的产生，但不促进 IL-10 的产生。在宫颈内膜细胞中没有表现出诱导作用。沙眼衣原体感染消除了阴茎尿道细胞中 CD1d 介导的细胞因子产生。 CD1d 介导的免疫反应的基础缺陷可能导致对性传播媒介的易感性。 CD1d 介导的信号传导减少可能有助于沙眼衣原体逃避先天免疫细胞的检测
Mucosal epithelia of the human lower reproductive tract (vagina, cervix, and penile urethra) are exposed to sexually transmitted microbes, including Chlamydia trachomatis. The in vivo susceptibility of each tissue type to infection with C. trachomatis is quite distinct. CD1d is expressed on the surface of antigen-presenting cells, including mucosal epithelial cells, and interacts specifically with invariant NKT cells. Invariant NKT cells play a role in both innate and adaptive immune responses to microbes. Here we assessed CD1d expression in normal reproductive tissues by using immunohistochemistry. Immortalized epithelial cell lines from the human lower reproductive tract (vagina, endocervix, and penile urethra) were examined for CD1d expression and for ligand-induced cytokine production induced by CD1d cross-linking. CD1d expression in normal tissue was strong in the vagina but weak in the endocervix and penile urethra. Gamma interferon exposure induced CD1d transcription in all of the cell types studied, with the strongest induction in vaginal cells. Flow cytometry revealed cell surface expression of CD1d in vaginal and penile urethral epithelial cells but not in endocervical cells. Ligation of surface-expressed CD1d by monoclonal antibody cross-linking promoted interleukin-12 (IL-12) and IL-15, but not IL-10, production in vaginal and penile urethral cells. No induction was demonstrated in endocervical cells. CD1d-mediated cytokine production in penile urethral cells was abrogated by C. trachomatis infection. Basal deficiency in CD1d-mediated immune responsiveness may result in susceptibility to sexually transmitted agents. Decreased CD1d-mediated signaling may help C. trachomatis evade detection by innate immune cells