Color Foundation, Landsmeer, the Netherlands.
Exp Dermatol. 2011 Feb;20(2):92-6. doi: 10.1111/j.1600-0625.2010.01200.x.
The 'Haptenation theory' concerns the multicausal pathogenesis of vitiligo ending ultimately in the (partial) disappearance of melanocytes from the skin and/or hairs. The melanocyte specificity is attributed to the tyrosinase-catalysed production of haptogenic ortho-quinones that covalently bind to tyrosinase or other melanosomal proteins to generate neo-antigens. These latter, in turn, trigger an immunological cascade resulting in a melanocyte-specific delayed-type hypersensitivity reaction that eliminates melanocytes and produces the characteristic depigmentation. This causal chain of events is critically discussed with special reference to factors modifying the process and the possible influence of various biochemical changes, such as raised levels of catecholamines and epidermal hydrogen peroxide, which have been reported to be associated with the onset of vitiligo. This all adds up to the typical vitiligo reaction pattern or syndrome, which demands a treatment strategy involving most of the already known therapies. Similar pathogenetic mechanisms might be engaged in the enhancement of cellular immunity (vaccination) against melanoma.
“半抗原化理论”涉及导致黑素细胞(部分)从皮肤和/或毛发中消失的白癜风多病因发病机制。黑素细胞的特异性归因于酪氨酸酶催化产生的半抗原性邻苯醌,这些邻苯醌与酪氨酸酶或其他黑素体蛋白共价结合,产生新抗原。这些新抗原反过来触发免疫级联反应,导致黑素细胞特异性迟发型超敏反应,从而消除黑素细胞并产生特征性的色素脱失。本文将重点讨论这一因果事件链,并特别参考了改变这一过程的因素以及各种生化变化(如儿茶酚胺水平升高和表皮过氧化氢)的可能影响,这些变化与白癜风的发病有关。所有这些都构成了典型的白癜风反应模式或综合征,这需要一种治疗策略,包括已经知道的大多数治疗方法。针对黑色素瘤的细胞免疫增强(疫苗接种)可能涉及类似的发病机制。