Ho J L, Badaro R, Hatzigeorgiou D, Reed S G, Johnson W D
Department of Medicine, Cornell University Medical College, New York, New York 10021.
Biotherapy. 1994;7(3-4):223-35. doi: 10.1007/BF01878488.
The genus Leishmania, an obligate intramacrophage parasite, causes a wide spectrum of clinical diseases. It is worldwide in distribution and causes 20 million new cases annually with an at risk population of approximately 1.5 billion persons. The most severe forms are associated with high morbidity, mortality and relapses with conventional therapy. The therapeutic issues and responses to standard and alternative therapies are reviewed. Recent developments in molecular biology and immunology methods employed in the study of leishmaniasis have defined an intricate interaction of the parasite with host immune system. Perturbation of the host immune responses may be part of the survival mechanisms of Leishmania. In murine model, the finding of T helper cells that differ by their panel of cytokines has allowed a more precise definition of immunopathogenesis of leishmaniasis. Preliminary data from leishmaniasis patients lend support to this concept of altered immunomodulation. Furthermore, the data from leishmaniasis patients lend support to this concept of altered enhancement of therapeutic response by interferon-gamma has provided a new approach for treatment of patients using recombinant cytokines and for the study of the disease. Current research for early diagnosis, alternative therapies and need for vaccines are reviewed in the context of the immunopathology of leishmaniasis.
利什曼原虫属是一种专性巨噬细胞内寄生虫，可引发多种临床疾病。其分布遍及全球，每年导致2000万新发病例，高危人群约达15亿人。最严重的形式与传统治疗中的高发病率、死亡率及复发相关。本文综述了治疗问题以及对标准疗法和替代疗法的反应。利什曼病研究中使用的分子生物学和免疫学方法的最新进展明确了寄生虫与宿主免疫系统之间复杂的相互作用。宿主免疫反应的紊乱可能是利什曼原虫生存机制的一部分。在小鼠模型中，发现细胞因子谱不同的辅助性T细胞使得对利什曼病免疫发病机制的定义更加精确。利什曼病患者的初步数据支持了这种免疫调节改变的概念。此外，利什曼病患者的数据支持了这种通过干扰素-γ改变治疗反应增强的概念，这为使用重组细胞因子治疗患者以及研究该疾病提供了一种新方法。本文在利什曼病免疫病理学的背景下综述了当前早期诊断、替代疗法的研究以及疫苗需求。
