Dept. of Pharmacology, Institute of Post Graduate Medical Education and Research, 244B AJC Bose Road, Kolkata 700020, India.
York Biomedical Research Institute, Hull York Medical School, University of York, Heslington, York, YO10 5DD, UK.
Trends Parasitol. 2023 Oct;39(10):822-836. doi: 10.1016/j.pt.2023.07.005. Epub 2023 Aug 15.
Post kala-azar dermal leishmaniasis (PKDL), a heterogeneous dermal sequela of visceral leishmaniasis (VL), is challenging in terms of its etiopathogenesis. Hypopigmentation is a consistent clinical feature in PKDL, but mechanisms contributing to the loss of melanocytes remains poorly defined. Like other hypopigmentary dermatoses - for example, vitiligo, psoriasis, and leprosy - the destruction of melanocytes is likely a multifactorial phenomenon, key players being immune dysregulation and inflammation. This review focuses on immunological mechanisms responsible for the 'murder' of melanocytes, prime suspects at the lesional sites being CD8 T cells and keratinocytes and their criminal tools being proinflammatory cytokines, for example, IFN-γ, IL-6, and TNF-α. Collectively, these may cause decreased secretion of melanocyte growth factors, loss/attenuation of cell adhesion molecules and inflammasome activation, culminating in melanocyte death.
无色素皮肤利什曼病（PKDL）是内脏利什曼病（VL）的一种异质性皮肤后遗症，其发病机制具有挑战性。色素减退是 PKDL 的一个一致的临床特征，但导致黑素细胞丧失的机制仍未明确定义。与其他色素减退性皮肤病 - 例如白癜风、银屑病和麻风病 - 一样，黑素细胞的破坏可能是一个多因素的现象，关键参与者是免疫失调和炎症。本综述重点介绍了负责“谋杀”黑素细胞的免疫学机制，病变部位的主要嫌疑犯是 CD8 T 细胞和角质形成细胞，它们的犯罪工具是促炎细胞因子，例如 IFN-γ、IL-6 和 TNF-α。总的来说，这些可能导致黑素细胞生长因子分泌减少、细胞黏附分子的丧失/减弱和炎症小体激活，最终导致黑素细胞死亡。
