自身免疫性介导的黑色素瘤中的许多面孔破坏了黑色素瘤
The many faces of autoimmune-mediated melanocyte destruction in melanoma
影响因子:5.90000
分区:医学2区 / 免疫学2区
发表日期:2024
作者:
Loredana Ungureanu, Alina Florentina Vasilovici, Salomea-Ruth Halmágyi, Ioana Irina Trufin, Adina Patricia Apostu, Simona Corina Şenilă
摘要
黑色素瘤是皮肤癌最严重的形式，其发病率在全球范围内增加。黑色素瘤细胞源自正常的黑素细胞并具有不同的黑素细胞特异性抗原，在白癜风中会产生免疫反应的相同抗原，这种抗原是白癜风，这种皮肤病是由自身免疫介导的黑素细胞破坏的特征。这篇综述的目的是介绍与黑色素瘤发育，进展和治疗相关的自身免疫性介导的黑素细胞破坏。白癜风患者似乎患有黑色素瘤的机会较低。另一方面，即使在原发性肿瘤的遥远部位，黑色素瘤患者也可以发育不良病变，该病变被定义为与黑色素瘤相关的白细胞病（MAL）。在接受免疫疗法或靶向疗法治疗的黑色素瘤患者中还描述了与药物相关的白细胞（DAL），这似乎是一个有利的预后因素。在临床上，MAL和DAL可以被诊断为白癜风，这三个实体之间几乎没有差异。在这篇综述中，在文献中研究了用不同疗法治疗的黑色素瘤患者的DAL发生率，并记录了患者的结果，研究表明，在黑色素瘤DAL患者中无疾病的生存期延长，接受了免疫检查点抑制剂治疗。但是，需要进一步的研究来了解自身免疫介导的黑素细胞破坏的动力学。
Abstract
Melanoma is the most severe form of skin cancer with an incidence that is increasing all over the world. Melanoma cells derive from normal melanocytes and share different melanocyte-specific antigens, the same antigens against which an immune reaction develops in vitiligo, a skin disease characterized by autoimmune-mediated melanocyte destruction. The purpose of this review is to present the autoimmune-mediated melanocyte destruction associated with melanoma development, progression and treatment. Patients with vitiligo seem to have a lower chance of developing melanoma. On the other hand, patients with melanoma can develop depigmented lesions even at distant sites from the primary tumor, defined as melanoma-associated leukoderma (MAL). Drug-associated leukoderma (DAL) was also described in melanoma patients treated with immunotherapy or targeted therapy and it seems to be a favorable prognostic factor. Clinically, MAL and DAL can be diagnosed as vitiligo and there are few differences between these three entities. In this review, the incidence of DAL in melanoma patients treated with different therapies was researched in the literature and patient outcome was recorded, with studies showing a prolonged disease-free survival in melanoma patients with DAL, treated with immune checkpoint inhibitors. Further studies are however needed to understand the dynamics of autoimmune-mediated melanocyte destruction.