前沿：自身免疫性皮肤病中朗格汉斯树突状细胞的迁移受损。
Cutting edge: migration of langerhans dendritic cells is impaired in autoimmune dermatitis.
作者信息
Eriksson Anna U, Singh Ram Raj
机构信息
Department of Medicine, Laboratory Medicine, Autoimmunity and Tolerance Laboratory, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
出版信息
J Immunol. 2008 Dec 1;181(11):7468-72. doi: 10.4049/jimmunol.181.11.7468.
Abstract
Tissue-resident dendritic cells, such as Langerhans cells (LC), normally carry Ags from tissues to lymph nodes to induce immunity to tissue Ags. In this study, we report that LC are reduced in the skin-draining lymph nodes of MRL-Fas(lpr/lpr) and MRL-Fas(+/+) mice that develop T cell-mediated autoimmune skin inflammation as compared with MHC-matched healthy strains. This deficiency of LC in skin-draining lymph nodes is due to a profound impairment of LC migration, resulting in the accumulation of activated LC in the skin. Such a defect in LC migration develops before the onset of skin lesions and correlates with the onset and severity of dermatitis. The reduced, rather than increased, migration of LC from skin to skin-draining lymph nodes represents a novel functional abnormality of LC in autoimmune dermatitis.
摘要
组织驻留树突状细胞，如朗格汉斯细胞（LC），通常将抗原从组织携带至淋巴结，以诱导对组织抗原的免疫反应。在本研究中，我们报告称，与 MHC 匹配的健康品系相比，发生 T 细胞介导的自身免疫性皮肤炎症的 MRL-Fas(lpr/lpr)和 MRL-Fas(+/+)小鼠引流皮肤的淋巴结中的 LC 减少。引流皮肤的淋巴结中 LC 的这种缺乏是由于 LC 迁移严重受损，导致活化的 LC 在皮肤中积聚。LC 迁移的这种缺陷在皮肤病变发作之前就已出现，并与皮炎的发作和严重程度相关。LC 从皮肤向引流皮肤的淋巴结迁移减少而非增加，代表了自身免疫性皮炎中 LC 的一种新的功能异常。
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