Apoptosis induced by HIV‐gp120 in a Th1 clone involves the generation of reactive oxygen intermediates downstream CD95 triggering

FEBS Letters

Colombo, Mario P.²  Accornero, Paola²  Delia, Domenico¹  Kurrle, Roland³  Radrizzani, Marina² 

[1] Division of Experimental Oncology A, Istituto Nazionale Tumori, Milano, Italy;Division of Experimental Oncology D, Istituto Nazionale Tumori, via Venezian 1, 20133 Milano, Italy;Behringwerke AG, Marburg, Germany

关键词: HIV;    gp120;    Apoptosis;    ROI;    PTK;    CD4+ Th1 clone;    TUNEL;    terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling;    DHR;    dihydrorhodamine-123;    MFI;    mean fluorescence intensity;    PTK;    protein tyrosine kinase;    ROI;    reactive oxygen intermediates;   

DOI  :  10.1016/S0014-5793(97)00672-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

HIV-gp120 sensitizes Th1 clones from seronegative donors to apoptosis, which occurs through two distinct events: expression of CD95L followed by its interaction with CD95 to trigger cell death. gp120-apoptosis of the Th1 clone 103 was inhibited by Cyclosporin A, the PTK inhibitors Genistein and PNU152518, as well as the anti-oxidants Ascorbic Acid and Glutathione. Cyclosporin A interfered with CD95L expression, Ascorbic Acid and Glutathione inhibited cell death triggered by CD95/CD95L interaction; Genistein and PNU152518 acted on both steps. The occurrence of oxidative stress during CD95-dependent apoptosis was supported by the direct evidence of ROI production.

【 授权许可】

Unknown