Study on the role of lymphocytes on organ failure and disturbed host defense mechanism due to infection and stress

当给予OK 432或缺血刺激诱导肝窦内皮细胞凋亡时，以及当伴刀豆球蛋白A激活淋巴细胞时，肝窦内皮细胞可诱导灌注肝的急性损伤。在缺血肝脏中，来自肝细胞的过氧化氢诱导肝腺泡中部的窦状隙内皮细胞凋亡以及窦状隙内皮细胞中Hsp 72的表达。抗凋亡蛋白Bcl-2位于肝细胞线粒体的内膜和嵴上。Bcl-2的定位是不变的缺血challense.In严重感染和败血症的小鼠模型诱导随后的管理Ok 432和脂多糖，自然杀伤细胞和淋巴因子激活的杀伤细胞的活性升高，但淋巴细胞是非常敏感的Fas介导的凋亡。

Lympocytes may induce acute injuries of the perfused liver when sinusoidal endothelial cell apoptosis is induced by the administration of OK432 or ischemic challenge, and when lymphocytes are activated by concanavalin A. In the schemic liver, hydrogen peroxide derived from hepatocytes induces sisusoidal endothelial cell apoptosis in the midzone of Liver acinus as well as Hsp 72 expression in sinusoidal endothelial cells. An anti-apoptotic protein Bcl-2 is located in the inner membrane and crista of mitochondria in the hepatocytes. Localization of Bcl-2 is unchanged by the ischemic challenge.In a mouse model of severe infection and sepsis induced consequent administrations of Ok432 and lipopolysaccharide, both natural killer and lymphokine-activated killer activities are elevated, but lymphocytes are very sensitive to Fas-mediated apoptosis.