Brunet L R, Finkelman F D, Cheever A W, Kopf M A, Pearce E J
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
J Immunol. 1997 Jul 15;159(2):777-85.
To examine the role of the Th2-type response during schistosomiasis mansoni we compared disease progression in wild type (wt), and Th2-response deficient IL-4(-/-) mice. Whereas wt C57BL/6 mice tolerate infection and develop chronic disease, IL-4(-/-) C57BL/6 animals are highly susceptible, exhibiting severe acute cachexia followed by death. Data point toward morbidity in the IL-4(-/-) C57BL/6 mice being mediated by TNF-alpha, possibly through the uncontrolled production of nitric oxide in target organs such as the ileum. We propose that IL-4 prevents severe disease during schistosomiasis by regulating macrophage activation.
为研究2型辅助性T细胞（Th2）应答在曼氏血吸虫病中的作用，我们比较了野生型（wt）小鼠和缺乏Th2应答的白细胞介素4（IL-4）基因敲除（-/-）小鼠的疾病进展情况。野生型C57BL/6小鼠能够耐受感染并发展为慢性疾病，而IL-4基因敲除（-/-）的C57BL/6小鼠则高度易感，表现出严重的急性恶病质，随后死亡。数据表明，IL-4基因敲除（-/-）的C57BL/6小鼠的发病机制可能是由肿瘤坏死因子-α（TNF-α）介导的，可能是通过回肠等靶器官中一氧化氮的失控产生。我们认为，IL-4通过调节巨噬细胞的激活来预防血吸虫病期间的严重疾病。
