Kao C H, Yu H S
Department of Dermatology, Kaohsiung Medical Medical College, Taiwan, Republic of China.
J Dermatol. 1990 May;17(5):287-96. doi: 10.1111/j.1346-8138.1990.tb01643.x.
The role of Langerhans cells in the pathogenesis of nonsegmental type vitiligo is still unknown. In this study, biopsies were taken from 26 patients at various stages of nonsegmental type vitiligo and morphometrically observed to investigate the kinetics of Langerhans cells in patients at various stages of the disease. A marked depletion of OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with active nonsegmental type vitiligo. A repopulation of both OKT6-positive and ATPase-positive epidermal dendritic cells was noted in patients with stable nonsegmental type vitiligo. Profound depletion of epidermal OKT6-positive and ATPase-positive dendritic cells was noted in patients with repigmenting nonsegmental type vitiligo receiving treatments involving topical use of 0.05% Fluocinonide cream or PUVA photochemotherapy. Transmission electron microscopy confirmed the absence of epidermal dendritic cells (Langerhans cells and intermediate cells) in patients with active and repigmenting nonsegmental type vitiligo. In active nonsegmental type vitiligo, two possible explanations are proposed for the depletion of OKT6-positive and ATPase-positive epidermal dendritic cells (presumptive Langerhans cells): 1) the cells are destroyed by cytotoxic factors released during the course of destruction of melanocytes in active vitiligo, and/or 2) they leave the epidermis and migrate to regional lymph nodes to present certain antigens which are released from certain destroyed epidermal cells (keratinocytes or melanocytes) during the course of active vitiligo. The repopulated epidermal Langerhans cells may result from phenotypically transformed dermal dendritic cells in the depigmented lesions of patients with stable vitiligo. Since various therapies which result in repigmentation deplete the density of epidermal Langerhans cells markedly, it is suggested that depletion of epidermal Langerhans cells in stable vitiligo may aid in repigmentation. It is also proposed that the repopulated epidermal Langerhans cells may play a role in inhibiting the proliferation of epidermal melanocytes in depigmented lesions of stable vitiligo, thus various methods of treatment which deplete the Langerhans cells may eventually aid in the repigmentation of nonsegmental type vitiligo.
朗格汉斯细胞在非节段型白癜风发病机制中的作用仍不清楚。在本研究中,从26例处于非节段型白癜风不同阶段的患者身上取活检组织,并进行形态学观察,以研究疾病不同阶段患者朗格汉斯细胞的动力学变化。在活动期非节段型白癜风患者中,观察到OKT6阳性和ATP酶阳性的表皮树突状细胞明显减少。在稳定期非节段型白癜风患者中,OKT6阳性和ATP酶阳性的表皮树突状细胞均有重新聚集。在接受外用0.05%氟轻松乳膏或补骨脂素光化学疗法(PUVA)治疗的复色期非节段型白癜风患者中,观察到表皮OKT6阳性和ATP酶阳性树突状细胞显著减少。透射电子显微镜证实,活动期和复色期非节段型白癜风患者的表皮树突状细胞(朗格汉斯细胞和中间细胞)缺失。对于活动期非节段型白癜风患者中OKT6阳性和ATP酶阳性表皮树突状细胞(推测为朗格汉斯细胞)的减少,提出了两种可能的解释:1)这些细胞在活动期白癜风黑素细胞破坏过程中被释放的细胞毒性因子破坏,和/或2)它们离开表皮并迁移至区域淋巴结,以呈递在活动期白癜风过程中从某些被破坏的表皮细胞(角质形成细胞或黑素细胞)释放的某些抗原。重新聚集的表皮朗格汉斯细胞可能源于稳定期白癜风患者色素脱失皮损中表型转化的真皮树突状细胞。由于各种导致复色的疗法会显著降低表皮朗格汉斯细胞的密度,因此提示稳定期白癜风中表皮朗格汉斯细胞的减少可能有助于复色。还提出重新聚集的表皮朗格汉斯细胞可能在抑制稳定期白癜风色素脱失皮损中表皮黑素细胞的增殖中起作用,因此,各种消耗朗格汉斯细胞的治疗方法最终可能有助于非节段型白癜风的复色。