无法产生白细胞介素-4或白细胞介素-10的小鼠对结核分枝杆菌感染表现出正常的抵抗力。
Mice incapable of making IL-4 or IL-10 display normal resistance to infection with Mycobacterium tuberculosis.
作者信息
North R J
机构信息
The Trudeau Institute, Saranac Lake, NY 12983, USA.
出版信息
Clin Exp Immunol. 1998 Jul;113(1):55-8. doi: 10.1046/j.1365-2249.1998.00636.x.
Abstract
With a view to determining whether production of Th2 cytokines, IL-4 or IL-10, is responsible for the inability of mice to resolve infection with Mycobacterium tuberculosis, mice with targeted disruption of their IL-4 or IL-10 gene were compared with wild-type mice in terms of their ability to defend against an M. tuberculosis infection initiated via the respiratory route. The results show that mice that are unable to make either IL-4 or IL-10 are no more capable than wild-type mice at defending against tuberculosis (TB). Therefore, the results are inconsistent with the proposition that the inadequacy of Th1-mediated anti-tuberculosis immunity is due to its down-regulation by either of these Th2 cytokines.
摘要
为了确定Th2细胞因子IL-4或IL-10的产生是否是小鼠无法清除结核分枝杆菌感染的原因，将IL-4或IL-10基因靶向破坏的小鼠与野生型小鼠在抵御经呼吸道引发的结核分枝杆菌感染的能力方面进行了比较。结果表明，无法产生IL-4或IL-10的小鼠在抵御结核病（TB）方面并不比野生型小鼠更有能力。因此，这些结果与Th1介导的抗结核免疫不足是由于这些Th2细胞因子中的任何一种对其下调这一观点不一致。
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