Biology of Langerhans cells: analysis by experiments to deplete Langerhans cells from human skin.
Biology of Langerhans cells: analysis by experiments to deplete Langerhans cells from human skin.
复制标题
朗格汉斯细胞生物学：通过实验分析从人体皮肤中去除朗格汉斯细胞。
DOI：
10.1111/1523-1747.ep12261453
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Emam,M
中科院分区：
文献类型：
--
作者：
Krueger,GG;Emam,M
体内研究已经证明，各种皮肤治疗，例如，紫外线照射，局部皮质类固醇，胶带剥离，将暂时耗尽表皮朗格汉斯细胞（LC）。这种损失是否仅仅代表LC特有的细胞表面标志物的损失，或细胞的实际消耗，是未知的。通过设计，移植到先天性无胸腺（裸）小鼠的正常人皮肤是一个缺乏人LC循环前体的系统。由于LC已被证明是骨髓来源的，因此该系统中这些细胞的任何消耗都应该是永久性的。移植后，大剂量紫外线照射（400 mJ/cm ~ 2，每48 h，× 3），高剂量皮质类固醇激素（2.5 mg戊酸倍他米酯/cm ~ 2，每天，× 5），胶带剥离（× 20）。移植前的处理包括：（a）用900 R γ射线处理供体皮肤，（B）补体固定LC Ia样抗原的单克隆抗体，然后是新鲜补体，（c）与毒素结合的单克隆抗体。使用免疫诊断试剂抗HLA-DR和表面胞外酶ATPase.Results定量分析了对照和治疗的表皮片上LC的数量，结果表明，UV照射和局部皮质类固醇通过这些分析减少了LC的数量。然而，在3周内，恢复到治疗前水平。X射线照射和胶带剥离无影响。尽管有证据表明单克隆抗体、补体和毒性系统被递送至表皮内的LC，但没有证据表明这些治疗导致LC减少。看来，LC目前是长寿或取代本地从增殖池和某些细胞膜决定因素的人LC有点差异敏感的紫外线辐射和皮质类固醇。
In vivo studies have demonstrated that various treatments of skin, e.g., UV irradiation, topical corticosteroids, and tape-stripping, will temporarily deplete the epidermis of Langerhans cells (LC). Whether this loss represents simply a loss of cell surface markers unique to LC, or actual depletion of cells, is unknown. By design, normal human skin transplanted to the congenitally athymic (nude) mouse is a system devoid of circulating precursors for human LC. Because LC have been shown to be of bone marrow origin, any depletion of these cells in this system should be permanent. Treatments to deplete LC from human skin grafts on nude mice after grafting included: (a) large doses of UV radiation (400 mJ/cm2every 48 h, × 3), (b) potent high-dose topical corticosteroids (2.5 mg betamethasone valerate/cm2every day, × 5), (c) tape-stripping (× 20). Treatments before grafting included: (a) treating donor skin with 900 R of gamma irradiation, (b) complement fixing monoclonal antibody to Ia-like antigens of LC, followed by fresh complement, (c) monoclonal antibody conjugated to toxins. Quantitation of the number of LC was analyzed on control and treated epidermal sheets using immunodiagnostic reagents, anti-HLA-DR, and surface ectoenzymes, ATPase.Results show that both UV irradiation and topical corticosteroids reduce the number of LC by these analyses. However, within 3 weeks, recovery to pretreatment levels has occurred. X-irradiation and tape-stripping were without effect. Despite evidence that the monoclonal antibody, complement, and toxic systems were delivered to the LC within the epidermis, there is no evidence that these treatments resulted in a decrease in LC. It appears that LC are currently either long-lived or replaced locally from a proliferative pool and that certain cell membrane determinants of human LC are somewhat differentially sensitive to UV radiation and corticosteroids.