Epidermal Langerhans cell-deficient mice develop enhanced contact hypersensitivity
Epidermal Langerhans cell-deficient mice develop enhanced contact hypersensitivity
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DOI：
10.1016/j.immuni.2005.10.008
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发表时间：
2005-12-01
期刊：
影响因子：
32.4
通讯作者：
Shlomchik, MJ
中科院分区：
文献类型：
--
作者：
Kaplan, DH;Jenison, MC;Shlomchik, MJ
表皮朗格汉斯细胞（LCs）是一种独特的皮肤树突状细胞群，在皮肤中获得抗原并迁移到引流淋巴结，在那里它们被认为是启动适应性免疫反应。为了研究LCs在皮肤免疫中的功能需求，我们培育了BAC转基因小鼠，在这些小鼠中，使用来自人Langerin的调节元件来驱动白喉毒素的表达。由此产生的小鼠具有组成性和持久性的表皮LCs缺失，但其他方面完好无损。出乎意料的是，我们发现接触性超敏反应（CHS）在没有接触性超敏反应的情况下被放大而不是消除。此外，我们发现LCs在启动阶段而不是效应阶段起作用。因此，LCs不仅对CHS是不可缺少的，而且它们还起到调节反应的作用，这是一种以前未被认识到的功能。
Epidermal Langerhans cells (LCs), a distinct skin-resident dendritic cell population, acquire antigen in the skin and migrate to draining lymph nodes where they are thought to initiate adaptive immune responses. To examine the functional requirement of LCs in skin immunity, we generated BAC transgenic mice in which the regulatory elements from human Langerin were used to drive expression of diphtheria toxin. The resulting mice have a constitutive and durable absence of epidermal LCs but are otherwise intact. Unexpectedly, we found that contact hypersensitivity (CHS) was amplified rather than abrogated in the absence of LCs. Moreover, we showed that LCs act during the priming and not the effector phase. Thus, LCs not only were dispensable for CHS, but they served to regulate the response, a previously unappreciated function.