Mukherjee Shibabrata, Mukhopadhyay Debanjan, Braun Claudia, Barbhuiya Joyashree N, Das Nilay K, Chatterjee Uttara, von Stebut Esther, Chatterjee Mitali
Department of Pharmacology, Institute of Postgraduate Medical Education and Research, Kolkata, India.
Exp Dermatol. 2015 Mar;24(3):232-4. doi: 10.1111/exd.12635.
Post kala-azar dermal leishmaniasis (PKDL) is the dermal sequel of visceral leishmaniasis (VL) and occurs after apparent cure or alongside with VL. It is confined to South Asia (India, Nepal and Bangladesh) and East Africa (mainly Sudan), the incidence being 5-10% and 50-60% respectively. In South Asia, as the transmission of VL is anthroponotic, PKDL patients are the proposed disease reservoir, thus assuming epidemiological significance, its eradication being linked to the control of leishmaniasis. In the absence of an animal model and its low incidence, factors contributing towards the immunopathogenesis of PKDL remain an open-ended, yet pertinent question. This study delineated the lesional immunopathology in terms of granuloma formation, Langerhans cells, tissue macrophages along with mRNA expression of IL-12p40 and IL-10. Our study in Indian PKDL for the first time identified that the number of CD1a(+) /CD207(+) Langerhans cells are decreased and CD68(+) macrophages are increased along with the absence of an epitheloid granuloma. Importantly, this decrease in Langerhans cells was associated with decreased mRNA expression of IL-12p40 and increased IL-10. This was reverted with treatment allowing for elimination of parasites and disease resolution along with an increase in Langerhans cells and decrease in macrophages. Thus, in Indian PKDL, absence of a granuloma formation along with a decrease in Langerhans cells collectively caused immune inactivation essential for parasite persistence and disease sustenance.
黑热病后皮肤利什曼病（PKDL）是内脏利什曼病（VL）的皮肤后遗症，发生在表面治愈后或与VL同时出现。它局限于南亚（印度、尼泊尔和孟加拉国）和东非（主要是苏丹），发病率分别为5%-10%和50%-60%。在南亚，由于VL的传播是人间传播，PKDL患者被认为是疾病储存宿主，因此具有流行病学意义，其根除与利什曼病的控制相关。由于缺乏动物模型且发病率低，导致PKDL免疫发病机制的因素仍然是一个悬而未决但相关的问题。本研究从肉芽肿形成、朗格汉斯细胞、组织巨噬细胞以及IL-12p40和IL-10的mRNA表达方面描述了病变的免疫病理学。我们在印度PKDL患者中的研究首次发现，CD1a(+)/CD207(+)朗格汉斯细胞数量减少，CD68(+)巨噬细胞数量增加，同时缺乏上皮样肉芽肿。重要的是，朗格汉斯细胞的这种减少与IL-12p40的mRNA表达降低和IL-10增加有关。治疗后这种情况得到逆转，寄生虫被清除，疾病得到缓解，同时朗格汉斯细胞增加，巨噬细胞减少。因此，在印度PKDL中，缺乏肉芽肿形成以及朗格汉斯细胞减少共同导致了免疫失活，这对寄生虫持续存在和疾病维持至关重要。
