Ismail A, El Hassan A M, Kemp K, Gasim S, Kadaru A E, Moller T, Kharazmi A, Theander T G
Centre for Medical Parasitology, Institute of Medical Microbiology and Immunology, University of Copenhagen, Denmark.
J Pathol. 1999 Dec;189(4):615-22. doi: 10.1002/(SICI)1096-9896(199912)189:4<615::AID-PATH466>3.0.CO;2-Z.
In Sudan, post kala-azar dermal leishmaniasis (PKDL) caused by Leishmania donovani develops in half of the patients treated for visceral leishmaniasis (kala-azar). In most patients lesions heal spontaneously, but in others symptoms are severe and persist for years. This study examined the immunological response in lesions of PKDL patients by immunohistochemistry and compared the findings with results obtained using peripheral blood mononuclear cells (PBMCs). In all lesions, parasites or parasite antigen were present and provoked the formation of an inflammatory infiltrate consisting of a mixture of macrophages, lymphocytes, and plasma cells. In patients who had high interferon-gamma (IFNgamma) responses to Leishmania antigen in vitro, compact epithelioid granulomas were formed. The inflammatory cells were mainly CD3(+) and interleukin-10 (IL10) was the most prominent cytokine in the lesions. However, IFNgamma was found in all and IL4 in most lesions, in varying amounts. PBMCs from all patients responded to Leishmania antigen by IFNgamma production or proliferation. The results indicate that PKDL develops as a result of an influx of immunocompetent cells into skin, which harbours parasites. The inflammatory response to the parasites is complex. It involves several cell types and cytokines, of which some are antagonistic. It is conceivable that the balance between these cytokines determines the outcome of the disease.
在苏丹，由杜氏利什曼原虫引起的黑热病后皮肤利什曼病（PKDL）发生在一半接受内脏利什曼病（黑热病）治疗的患者中。大多数患者的皮损会自发愈合，但其他患者的症状严重且会持续数年。本研究通过免疫组织化学检查了PKDL患者皮损中的免疫反应，并将结果与使用外周血单个核细胞（PBMC）获得的结果进行比较。在所有皮损中，均存在寄生虫或寄生虫抗原，并引发了由巨噬细胞、淋巴细胞和浆细胞混合组成的炎性浸润。在体外对利什曼原虫抗原有高干扰素-γ（IFNγ）反应的患者中，形成了致密的上皮样肉芽肿。炎性细胞主要为CD3(+)，白细胞介素-10（IL10）是皮损中最突出的细胞因子。然而，在所有皮损中均发现了IFNγ，大多数皮损中也发现了IL4，含量各不相同。所有患者的PBMC通过产生IFNγ或增殖对利什曼原虫抗原作出反应。结果表明，PKDL是由于免疫活性细胞流入寄生有寄生虫的皮肤而发生的。对寄生虫的炎症反应很复杂。它涉及多种细胞类型和细胞因子，其中一些具有拮抗作用。可以想象，这些细胞因子之间的平衡决定了疾病的转归。
