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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.

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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