Kanagawa O, Vaupel B A, Korsmeyer S J, Russell J H
Department of Pathology, Washington School of Medicine, St. Louis, MO 63110, USA.
Eur J Immunol. 1995 Sep;25(9):2421-7. doi: 10.1002/eji.1830250902.
Murine acquired immunodeficiency syndrome (MAIDS) is caused by a defective murine leukemia virus. The disease is characterized by abnormal lymphoproliferation, impaired T and B cell function and aberrant regulation of cytokines. Both T and B lymphocytes show activated phenotypes, but undergo apoptotic death with characteristic DNA fragmentation. These results indicate the presence of a continuous activation death pathway of the lymphocytes in MAIDS. Overexpression of the bcl-2 transgene in lymphocytes showed no effect on the apoptotic cell death or on the development of the disease. In contrast, mice carrying mutations in either Fas or Fas ligand exhibited accelerated progression of the disease upon infection with MAIDS virus. These results suggest the involvement of Fas-Fas ligand system in the pathogenesis of MAIDS.
小鼠获得性免疫缺陷综合征(MAIDS)由一种缺陷型小鼠白血病病毒引起。该疾病的特征为异常的淋巴细胞增殖、T细胞和B细胞功能受损以及细胞因子调节异常。T淋巴细胞和B淋巴细胞均表现出活化表型,但会经历伴有特征性DNA片段化的凋亡死亡。这些结果表明在MAIDS中存在淋巴细胞的持续活化死亡途径。淋巴细胞中bcl-2转基因的过表达对凋亡细胞死亡或疾病发展没有影响。相反,Fas或Fas配体发生突变的小鼠在感染MAIDS病毒后疾病进展加速。这些结果提示Fas-Fas配体系统参与了MAIDS的发病机制。