Immune dysregulation and inflammation causing hypopigmentation in post kala-azar dermal leishmaniasis: partners in crime?
Immune dysregulation and inflammation causing hypopigmentation in post kala-azar dermal leishmaniasis: partners in crime?
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DOI：
10.1016/j.pt.2023.07.005
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发表时间：
2023-09-13
影响因子：
9.6
通讯作者：
Chatterjee，Mitali
中科院分区：
文献类型：
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作者：
Sengupta，Ritika;Roy，Madhurima;Chatterjee，Mitali
黑热病后皮肤利什曼病（PKDL）是内脏利什曼病（VL）的异质性皮肤后遗症，其发病机制具有挑战性。色素减退是PKDL的一贯临床特征，但导致黑素细胞丢失的机制仍不清楚。与其他色素减退性皮肤病（如白癜风、银屑病和麻风病）一样，黑素细胞的破坏可能是一种多因素现象，关键因素是免疫失调和炎症。本文综述了黑素细胞被“谋杀”的免疫学机制，病变部位的主要嫌疑人是CD 8 +T细胞和角质形成细胞，其犯罪工具是促炎细胞因子，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的分泌减少，细胞粘附分子的损失/衰减和炎性小体活化，最终导致黑素细胞死亡。
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.