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登革病毒诱导的细胞毒性因子处理后对人血白细胞E-玫瑰花结形成和吞噬作用的抑制

Inhibition of E-rosette formation and phagocytosis by human blood leucocytes after treatment with the dengue virus-induced cytotoxic factor.

作者信息

Chaturvedi U C, Gulati L, Mathur A

出版信息

Immunology. 1982 Apr;45(4):679-85.

Abstract

We have observed earlier that T lymphocytes of dengue type 2 virus (DV)-infected mouse spleen produce a cytotoxic factor (CF) which kills T lymphocytes and macrophages of the spleen of normal mice or animals of other species. In the present study an effort was made to study the effect of CF treatment on human peripheral blood leucocytes. After treatment with various dilutions of CF at 4 degrees for 1 hr 25%-36% of T lymphocytes lost their capacity to form E rosettes and 25%-36% of monocytes lost their phagocytic function. Cytotoxic-factor treatment had no effect on formation of EAC rosettes by B lymphocytes and the phagocytic functions of polymorphonuclear cells. Pretreatment of cells with 2,4 dinitrophenol, reduced glutathione or ouabain, which act on the cell membrane, inhibited the effect of CF on E-rosette formation and phagocytosis. This indicated that CF acts by inducing changes in the cell membrane. It is likely that production of a similar factor in DV-infected humans is responsible for similar alterations observed in their blood.

摘要

我们先前观察到,感染登革2型病毒(DV)的小鼠脾脏T淋巴细胞产生一种细胞毒性因子(CF),该因子可杀死正常小鼠或其他物种动物脾脏中的T淋巴细胞和巨噬细胞。在本研究中,我们致力于研究CF处理对人外周血白细胞的影响。用不同稀释度的CF在4℃处理1小时后,25%-36%的T淋巴细胞失去形成E花环的能力,25%-36%的单核细胞失去吞噬功能。细胞毒性因子处理对B淋巴细胞形成EAC花环以及多形核细胞的吞噬功能没有影响。用作用于细胞膜的2,4-二硝基苯酚、还原型谷胱甘肽或哇巴因对细胞进行预处理,可抑制CF对E花环形成和吞噬作用的影响。这表明CF通过诱导细胞膜变化起作用。在感染DV的人类中产生类似因子可能是其血液中观察到类似改变的原因。

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