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抗巨噬细胞表面分子Mac-1单克隆抗体对利什曼原虫入侵巨噬细胞的抑制作用
引用本文:薛长贵,杨柳萍,崔晶. 抗巨噬细胞表面分子Mac-1单克隆抗体对利什曼原虫入侵巨噬细胞的抑制作用[J]. 地方病通报, 1997, 0(2)
作者姓名:薛长贵  杨柳萍  崔晶
作者单位:河南医科大学寄生虫学教研室!郑州市,450052,河南医科大学寄生虫学教研室!郑州市,450052,河南医科大学寄生虫学教研室!郑州市,450052
摘    要:应用抗巨噬细胞表面分子Mac-1单克隆抗体(M1/70和M18/2)处理巨噬细胞,观察M1/70和M18/2对杜氏利曼原虫前鞭毛体入侵巨噬细胞的抑制作用。结果,经上述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及速度也减慢。M1/70和M18/2两种单抗同时应用,则对原虫侵入巨噬细胞的抑制作用更为显著,巨噬细胞受染率为13.8%,且受染巨噬细胞内入侵的原虫数量大多仅有1~2个。提示,M1/70和M18/2单克隆抗体可以通过与巨噬细胞表面Mac-1的结合,干扰巨噬细胞表面分子上与利什曼原虫相结合的连接位点,抑制利什曼原虫对巨噬细胞的入侵。

关 键 词:利什曼原虫  巨噬细胞  补体受体

Inhibition of Phagocytosis of Leishmania Parasites to Macrophages by Anti-macrophage Surface Molecule Mac-1 Monoclonal Antibodies
Xue Changgui, Yang Liuping, Cui Jing. Inhibition of Phagocytosis of Leishmania Parasites to Macrophages by Anti-macrophage Surface Molecule Mac-1 Monoclonal Antibodies[J]. Endemic Diseases Bulletin, 1997, 0(2)
Authors:Xue Changgui   Yang Liuping   Cui Jing
Abstract:The role of anti-macrophage surface molecule Mac-l monoclonal antibodies, M1/70 and M18/2,in the phagocytosis of Leishmania donovani to macrophages was investigatedby treating macrophages with M1/70 and M18/2. The results shoued that after the macrophages were treated 3O min withM1/70, or (and) M18/2,the infected macrophage percentage and the parasite numbers in infected macrophages were decreased and the phagocytic process of the parasite into macrophages was decelerated. While macrophages were treated by using bothM1/70 and M18/2, the phagocytosis of the parasite to the macrophages was more obviously inhibited than the macrophages treated by either M1/70 or M18/2. The percentage of the infected macrophages was 13.8% and there only were 1~2 parasites in per infected macrophage. These data indicated that M1/70 and M18/2might inhibit the phagocytosis of leishmaniaparasites to macrophages by interference of the binding site of macrophage surfacemolecule for leishmania parasites in the interaction between the antibodies and macrophage surface Mac-l.
Keywords:Leishmania  Macrophages  Complement receptors
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