Palkowski M R, Nordlund M L, Rheins L A, Nordlund J J
Arch Dermatol. 1987 Aug;123(8):1022-8.
The C57Bl/Ler-vit.vit mouse grows a black pelage after birth. During successive hair molts, the fur loses its pigmentation. By 6 months of age, most of the fur of the animal is white. The epidermis of the ears and tail also loses its pigmentation. Histologic studies confirm that in the epidermis and hair follicles there is an absence of pigment cells identifiable by various histochemical or electron microscopic techniques. This mouse may be an excellent model in which to study the role of Langerhans' cells and the immune response in the pathogenesis of vitiligo, a study not easily done in humans. From results of prior studies, we postulated that if Langerhans' cells were involved in the destruction of melanocytes, they would be abnormal (either more or less numerous) in number during the active phase of depigmentation and normal in number after depigmentation was complete. To determine whether the Langerhans cell (Ia+/adenosine triphosphatase dendritic epidermal cell) might be involved in destruction of pigment cells, we quantified the number of Ia+ and adenosine triphosphatase dendritic cells in the hair follicles in skin from the ear, abdomen, back, and tail from male C57Bl/Ler-vit.vit mice while the fur and skin were depigmenting and after depigmentation was almost completed. We found that Langerhans' cells were normal in number during depigmentation and were most numerous after depigmentation. Previous studies indicate that Langerhans' cells in these mice are functionally defective and respond poorly to some contact allergens. From these morphologic and functional data, we conclude that Langerhans' cells probably are uninvolved in causing depigmentation in these mice. We also observed that the epithelium of hair follicles has a significantly higher (up to 1600/mm2) population density of Langerhans' cells than interfollicular skin.
C57Bl/Ler-vit.vit小鼠出生后毛发变黑。在连续换毛期间，毛发失去色素沉着。到6个月大时，该动物的大部分毛发变为白色。耳朵和尾巴的表皮也失去色素沉着。组织学研究证实，在表皮和毛囊中，通过各种组织化学或电子显微镜技术无法识别出色素细胞。这种小鼠可能是研究朗格汉斯细胞和免疫反应在白癜风发病机制中作用的极佳模型，而这一研究在人类中不易进行。根据先前的研究结果，我们推测，如果朗格汉斯细胞参与黑素细胞的破坏，那么在色素脱失的活跃期它们数量会异常（要么增多要么减少），而在色素脱失完全后数量正常。为了确定朗格汉斯细胞（Ia + /三磷酸腺苷树突状表皮细胞）是否可能参与色素细胞的破坏，我们对雄性C57Bl/Ler-vit.vit小鼠耳朵、腹部、背部和尾巴皮肤毛囊中的Ia + 和三磷酸腺苷树突状细胞数量进行了量化，观察时间为毛发和皮肤色素脱失期间以及色素脱失几乎完成后。我们发现，在色素脱失期间朗格汉斯细胞数量正常，色素脱失后数量最多。先前的研究表明，这些小鼠中的朗格汉斯细胞功能存在缺陷，对某些接触性过敏原反应较差。根据这些形态学和功能数据，我们得出结论，朗格汉斯细胞可能未参与这些小鼠的色素脱失过程。我们还观察到，毛囊上皮中朗格汉斯细胞的群体密度（高达1600/mm²）显著高于毛囊间皮肤。
