Vuitton Dominique Angèle, Zhang Shao Ling, Yang Yurong, Godot Véronique, Beurton Isabelle, Mantion Georges, Bresson-Hadni Solange
WHO Collaborating Centre for Prevention and Treatment of Human Echinococcosis, Université de Franche-Comté and University Hospital, Besançon, France.
Parasitol Int. 2006;55 Suppl:S51-5. doi: 10.1016/j.parint.2005.11.007. Epub 2005 Dec 19.
As exemplified by "aborted" calcified liver lesions commonly found in patients from endemic areas, Echinococcus multilocularis metacestodes develop only in a minority of individuals exposed to infection with the papasite. Clinical research has disclosed some aspects of the survival strategy of E. multilocularis in human hosts. Clinical observations in liver transplantation and AIDS suggest that suppression of cellular/Th1-related immunity increases disease severity. Most of the studies have stressed a role for CD8+ T cells and for Interleukin-10 in the development of tolerance. A spontaneous secretion of IL-10 by the PBMC seems to be the immunological hallmark of patients with progressive forms of alveolar echinococcosis (AE). IL-10-induced inhibition of effector macrophages, but also of antigen-presenting dendritic cells, may be operating and allowing parasite growth and survival. The genetic correlates of susceptibility to infection with E. multilocularis are clearer in humans than in the mouse model. A significant link between MHC polymorphism and clinical presentation of AE has been shown, and the spontaneous secretion of IL-10 in patients with a progressive AE is higher in patients with the HLA DR3+, DQ2+ haplotype. Clustering of cases in certain families, in communities otherwise exposed to similar risk factors, also points to immuno-genetic predisposition factors that may allow the larva to escape host immunity more easily. The first stage of larval development may be crucial in producing "danger signals" stimulating the initial production of cytokines. Therapeutic use of Interferon alpha is an attempt to foil the survival strategy of E. multilocularis.
以流行地区患者中常见的“退化型”钙化肝损伤为例，多房棘球绦虫的中绦期幼虫仅在少数感染该寄生虫的个体中发育。临床研究揭示了多房棘球绦虫在人类宿主中的一些生存策略。肝移植和艾滋病的临床观察表明，细胞/Th1相关免疫的抑制会增加疾病的严重程度。大多数研究强调了CD8 + T细胞和白细胞介素-10在耐受性发展中的作用。外周血单核细胞自发分泌IL-10似乎是进行性肺泡型棘球蚴病（AE）患者的免疫标志。IL-10诱导效应巨噬细胞以及抗原呈递树突状细胞的抑制，可能在起作用并使寄生虫生长和存活。与小鼠模型相比，人类对多房棘球绦虫感染易感性的遗传相关性更为明确。已显示MHC多态性与AE临床表现之间存在显著联系，并且具有HLA DR3 +、DQ2 +单倍型的进行性AE患者中IL-10的自发分泌更高。在其他暴露于相似危险因素的社区中，某些家庭中病例的聚集也表明免疫遗传易感性因素可能使幼虫更容易逃避宿主免疫。幼虫发育的第一阶段在产生刺激细胞因子初始产生的“危险信号”方面可能至关重要。干扰素α的治疗用途是试图挫败多房棘球绦虫的生存策略。
