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目的：探索细胞内利什曼原虫的入侵、生存机制，为研制阻断利什曼原虫与巨噬细胞结合的新型抗利什曼药物以及利什曼病免疫预防和免疫治疗的研究提供理论基础。方法：采用抗Ｍａｃ１单克隆抗体（Ｍ１／７０和Ｍ１８／２）和重组的ＩＦＮγ，ＴＮＦα和ＩＬ３处理巨噬细胞，观察经上述因子处理后的巨噬细胞对杜氏利什曼原虫前鞭毛体入侵和无鞭毛体在细胞内生存的影响。结果：经Ｍ１／７０和Ｍ１８／２单抗处理后巨噬细胞对杜氏利什曼原虫的易感性明显降低，其原虫感染率和受染巨噬细胞内入侵的原虫数量减低，原虫对巨噬细胞的入侵过程和速度也减慢。Ｍ１／７０和Ｍ１８／２两种单抗同时应用，则对原虫入侵巨噬细胞的抑制作用更为显著。通过对实验中所用的三种细胞因子活化巨噬细胞能力的观察发现，重组的ＩＦＮγ或ＴＮＦα均可激活巨噬细胞，提高巨噬细胞的杀原虫活性，且上述两种细胞因子联合对巨噬细胞的活化具有协同增强作用。但重组的ＩＬ３不仅不能激活巨噬细胞而且尚抑制ＩＦＮγ对巨噬细胞的活化作用。通过测定活化巨噬细胞内氧化氮产物（ＮＯ２）的生成量，观察ＮＯ２生成与巨噬细胞对原虫杀伤活性的关系，进一步探索了活化巨噬细胞对细胞内原虫的杀伤机制。结论：作用于巨噬细?
OBJECTIVE: To explore the mechanism of invasion and survival of Leishmanii intracellular and to provide a theoretical basis for the development of new anti-Leishman drugs to block the combination of Leishmania and macrophages and immunological prevention and immunotherapy of leishmaniasis . Macrophages were treated with anti-Mac1 monoclonal antibody (M1 / 70 and M18 / 2) and recombinant IFNγ, TNFα and IL3, and observed the effect of macrophages treated with these factors on Duchenne Invasion of Leishmania promastigotes and the effect of amastigotes on intracellular survival. Results: The susceptibility of macrophages to Leishmania donovani significantly decreased after treatment with M1 / 70 and M18 / 2 mAbs. The infection rate of protozoa and the number of protozoal invaded by macrophages decreased. Cell invasion process and speed also slowed. The inhibition of protozoal invasion of macrophages was more significant when the two monoclonal antibodies M1 / 70 and M18 / 2 were applied at the same time. Through experiments on the ability of the three cytokines activated macrophages observed that the recombinant IFN γ or TNF α can activate macrophages to increase macrophage parasite activity and the above two cytokines The combination has a synergistic effect on the activation of macrophages. However, the recombinant IL 3 not only can not activate macrophages but also inhibit IFN γ on macrophage activation. The production of nitric oxide (NO2) in activated macrophages was measured to observe the relationship between NO2 production and cytotoxicity of protozoa to macrophages and to further explore the killing mechanism of activated macrophages on protozoa. Conclusion: The role of macrofine?