Inflammatory bowel disease requires the interplay between innate and adaptive immune signals

煽动性的碗疾病(IBD ) 是一种类型 1 个 T 助手房间(Th1 ) 调停了自体免疫的疾病。各种各样的研究表明了环境病原体也在这疾病的开始和前进起一个重要作用。有趣地， IBD 的致病被显示了与氮的氧化物有关(没有) 免除了天生的有免疫力的房间。尽管不被知道对内脏 epithelia 高度有毒，没有生产的规定有很小的信息，在 IBD 的病原学的一个主要问题是 Th1 房间和病原体怎么在 IBD 的正式就职交往。在现在的学习，我们集中于我们显示出的号码的规定巨噬细胞要求两 interferon-gamma (IFN-gamma ) ，这调停了并且为生产的调停 TLR4 的信号没有，它在肠并且随后引起发炎 IBD。因此， IBD 是天生的有免疫力的信号的一致行动的结果，例如到 TLR-4，和适应有免疫力的信号的 LPS 的绑定，例如 Th1 房间生产的 IFN-gamma。

Inflammatory bowl disease （IBD） is a type 1 T helper cell （Th1）-mediated autoimmune disease. Various studies have revealed that environmental pathogens also play a significant role in the initiation and progression of this disease. Interestingly, the pathogenesis of IBD has been shown to be related to nitric oxide （NO） released from innate immune cells. Although NO is known to be highly toxic to the gut epithelia, there is very little information about the regulation of NO production, One major question in the etiology of IBD is how Thl cells and pathogens interact in the induction of IBD. In present study, we focused on the regulation of NO. We show that macrophages require both interferon-γ, （IFN-γ）-mediated and TLR4-mediated signals for the production of NO, which causes inflammation in the intestine and subsequently IBD. Thus, IBD is the result of concerted actions of innate immune signals, such as the binding of LPS to TLR-4, and adaptive immune signals, such as IFN-γ produced by Thl cells.