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单苯佐卡因诱导的脱色:从酶阻断到自身免疫。

Monobenzone-induced depigmentation: from enzymatic blockade to autoimmunity.

机构信息

Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital Bonn, Bonn, Germany.

出版信息

Pigment Cell Melanoma Res. 2011 Aug;24(4):673-9. doi: 10.1111/j.1755-148X.2011.00878.x. Epub 2011 Jul 6.

DOI:10.1111/j.1755-148X.2011.00878.x
PMID:21689385
Abstract

Autoimmune side-effects such as vitiligo regularly occur during melanoma immunotherapy. As vitiligo development is associated with a superior prognosis, the active induction of vitiligo in melanoma patients can be a useful tactic. The potent skin-depigmenting agent monobenzone can be used successfully for this purpose. However, until recently, the mechanism of action behind monobenzone-induced skin depigmentation was unclear. Lately, the mechanistic basis for the augmented immunogenicity of monobenzone-exposed pigmented cells has been unveiled, and their active role in the induction of autoimmune T-cell-mediated vitiligo has become apparent. Here, we provide an immunological framework in which we condense this knowledge to an integrated theory of the generation of monobenzone-induced vitiligo.

摘要

自身免疫副作用,如白癜风,在黑色素瘤免疫治疗期间经常发生。由于白癜风的发展与较好的预后相关,因此在黑色素瘤患者中主动诱导白癜风可能是一种有用的策略。强效皮肤脱色剂单苯佐卡因可成功用于此目的。然而,直到最近,单苯佐卡因诱导皮肤脱色的作用机制仍不清楚。最近,单苯佐卡因暴露的色素细胞增强免疫原性的机制基础已经揭示,它们在诱导自身免疫性 T 细胞介导的白癜风中的积极作用也已经显现。在这里,我们提供了一个免疫学框架,将这些知识浓缩为单苯佐卡因诱导的白癜风产生的综合理论。

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Skin-depigmenting agent monobenzone induces potent T-cell autoimmunity toward pigmented cells by tyrosinase haptenation and melanosome autophagy.皮肤增白剂对苯二酚通过络合酪氨酸酶和自噬黑色素小体诱导针对色素细胞的强效 T 细胞自身免疫。
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