白细胞介素-18缺陷小鼠中自然杀伤细胞活性和辅助性T细胞1反应缺陷
Defective NK cell activity and Th1 response in IL-18-deficient mice.
作者信息
Takeda K, Tsutsui H, Yoshimoto T, Adachi O, Yoshida N, Kishimoto T, Okamura H, Nakanishi K, Akira S
机构信息
Department of Biochemistry, Hyogo College of Medicine, Nishinomiya, Japan.
出版信息
Immunity. 1998 Mar;8(3):383-90. doi: 10.1016/s1074-7613(00)80543-9.
IL-18 is a cytokine that is secreted from activated macrophages and induces IFNgamma production. To investigate the in vivo role of IL-18, we generated IL-18-deficient mice. In Propionibacterium acnes (P. acnes)-primed IL-18-deficient mice, LPS-induced IFNgamma production was markedly reduced, despite normal IL-12 induction. Natural killer cell activity was significantly impaired. Th1 cell response after injection of P. acnes or Mycobacterium bovis (bacillus Calmette-Guerin [BCG]) was significantly reduced. Similar results were observed in IL-12-deficient mice. Interestingly, Th1 response was induced after BCG infection in IL-12-deficient mice. We therefore generated mice lacking both IL-18 and IL-12. In these mice, NK activity and Th1 response were further impaired. This demonstrates the important role of both IL-18 and IL-12 in NK activity, as well as in in vivo Th1 response.
白细胞介素-18（IL-18）是一种由活化巨噬细胞分泌的细胞因子，可诱导γ干扰素（IFNγ）的产生。为了研究IL-18在体内的作用，我们培育出了IL-18基因缺陷型小鼠。在痤疮丙酸杆菌（P. acnes）致敏的IL-18基因缺陷型小鼠中，尽管白细胞介素-12（IL-12）的诱导正常，但脂多糖（LPS）诱导的IFNγ产生明显减少。自然杀伤细胞活性显著受损。注射痤疮丙酸杆菌或牛分枝杆菌（卡介苗[BCG]）后，Th1细胞反应明显减弱。在IL-12基因缺陷型小鼠中也观察到了类似结果。有趣的是，在IL-12基因缺陷型小鼠中，卡介苗感染后可诱导Th1反应。因此，我们培育出了同时缺乏IL-18和IL-12的小鼠。在这些小鼠中，自然杀伤细胞活性和Th1反应进一步受损。这证明了IL-18和IL-12在自然杀伤细胞活性以及体内Th1反应中的重要作用。
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