Ganguly Sudipto, Das Nilay Kanti, Panja Moumita, Pal Shekhar, Modak Dolanchampa, Rahaman Mehebubar, Mallik Sudeshna, Guha Subhashis Kamal, Pramanik Netai, Goswami Ramapada, Barbhuiya Joyashree Nath, Saha Bibhuti, Chatterjee Mitali
Department of Pharmacology, Institute of Postgraduate Medical Education and Research, Kolkata, India.
J Infect Dis. 2008 Jun 15;197(12):1762-71. doi: 10.1086/588387.
Post-kala-azar dermal leishmaniasis (PKDL), an established sequela of visceral leishmaniasis (VL), is proposed to facilitate anthroponotic transmission of VL, especially during interepidemic periods. Immunopathological mechanisms responsible for Indian PKDL are still poorly defined.
Our study attempted to characterize the immune profiles of patients with PKDL or VL relative to that of healthy control subjects by immunophenotyping, intracellular cytokine staining of peripheral blood mononuclear cells, and enzyme-linked immunosorbent assay for serum cytokines and immunoglobulin G (IgG) subclasses.
Patients with PKDL had significantly raised percentages of peripheral CD3+CD8+ cells compared with control subjects, a difference that persisted after cure. Patients with PKDL showed an intact response to phytohemagglutinin, with the percentages of lymphocytes expressing interferon (IFN)-gamma, interleukin (IL)-2, IL-4, and IL-10 being comparable to those in control subjects. Patients with VL had decreased IFN-gamma and IL-2 expression, which was restored after cure, and increased IL-10 expression, which persisted after cure. In their response to Leishmania donovani antigen, patients with PKDL showed a 9.6-fold increase in the percentage of IL-10-expressing CD3+CD8+ lymphocytes compared with control subjects, and this percentage decreased with treatment. Patients with PKDL had raised levels of IgG3 and IgG1 (surrogate markers for IL-10), concomitant with increased serum levels of IL-10.
IL-10-producing CD3+CD8+ lymphocytes are important protagonists in the immunopathogenesis of Indian PKDL.
黑热病后皮肤利什曼病（PKDL）是内脏利什曼病（VL）已确定的后遗症，被认为促进了VL的人传人传播，尤其是在流行间期。印度PKDL的免疫病理机制仍不清楚。
我们的研究试图通过免疫表型分析、外周血单个核细胞的细胞内细胞因子染色以及血清细胞因子和免疫球蛋白G（IgG）亚类的酶联免疫吸附测定，来描述PKDL或VL患者相对于健康对照者的免疫谱特征。
与对照者相比，PKDL患者外周血CD3+CD8+细胞百分比显著升高，治愈后这种差异仍然存在。PKDL患者对植物血凝素反应正常，表达干扰素（IFN）-γ、白细胞介素（IL）-2、IL-4和IL-10的淋巴细胞百分比与对照者相当。VL患者IFN-γ和IL-2表达降低，治愈后恢复，IL-10表达增加，治愈后持续存在。在对杜氏利什曼原虫抗原的反应中，与对照者相比，PKDL患者中表达IL-10的CD3+CD8+淋巴细胞百分比增加了9.6倍，且该百分比随治疗而降低。PKDL患者IgG3和IgG1（IL-10的替代标志物）水平升高，同时血清IL-10水平也升高。
产生IL-10的CD3+CD8+淋巴细胞是印度PKDL免疫发病机制中的重要参与者。
