细胞凋亡
肝炎
刀豆蛋白A
肿瘤坏死因子α
Fas配体
发病机制
免疫学
肝损伤
生物
干扰素γ
细胞因子
分子生物学
医学
程序性细胞死亡
内分泌学
体外
生物化学
作者
Yoh‐ichi Tagawa,Kenji Sekikawa,Yoichiro Iwakura
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:1997-08-01
卷期号:159 (3): 1418-1428
被引量:395
标识
DOI:10.4049/jimmunol.159.3.1418
摘要
Con A-induced hepatitis (Con A-hepatitis) is a hepatitis model in which hepatic injury is supposed to be caused by cytokines from activated T cells. To elucidate the pathogenesis of this disease, we analyzed the roles of IFN-gamma and TNF-alpha using deficient mice of these cytokines. Development of hepatitis was reduced significantly in IFN-gamma(-/-) mice, while susceptibility of TNF-alpha(-/-) mice was not changed. Interestingly, apoptotic cell death was observed in the affected livers of control or TNF-alpha(-/-) mice, but not in those of IFN-gamma(-/-) mice. Fas mRNA expression was increased in the livers of hepatitis mice, but less abundantly in those of IFN-gamma(-/-) mice. Since apoptosis of liver cells was rarely observed in Con A-treated lpr/lpr mice, involvement of the Fas-Fas ligand system in this apoptotic process was suggested. These observations suggest that IFN-gamma plays a central role in Con A-hepatitis by activating Fas-induced apoptosis of liver cells.
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