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首页> 外文期刊>Cell Research >Inflammatory bowel disease requires the interplay between innate and adaptive immune signals.
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Inflammatory bowel disease requires the interplay between innate and adaptive immune signals.

机译：炎症性肠病需要先天性和适应性免疫信号之间的相互作用。

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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 Th1 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-gamma (IFN-gamma)-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-gamma produced by Th1 cells.Cell Research (2006) 16: 70-74. doi:10.1038/sj.cr.7310009; published online 16 January 2006.
机译：炎性碗疾病（IBD）是1型T辅助细胞（Th1）介导的自身免疫性疾病。各种研究表明，环境病原体在该疾病的发生和发展中也起着重要作用。有趣的是，IBD的发病机制已显示与先天免疫细胞释放的一氧化氮（NO）有关。尽管已知NO对肠道上皮有剧毒，但关于NO产生调控的信息却很少。IBD病因中的一个主要问题是Th1细胞和病原体如何在IBD诱导中相互作用。在本研究中，我们集中于NO的调节。我们显示巨噬细胞需要干扰素-γ（IFN-γ）介导和TLR4介导的信号来产生NO，这会引起肠道炎症，并随后引起IBD。因此，IBD是先天免疫信号（例如LPS与TLR-4的结合）和适应性免疫信号（例如Th1细胞产生的IFN-γ）协同作用的结果.Cell Research（2006）16：70-74 。 doi：10.1038 / sj.cr.7310009;在线发布于2006年1月16日。

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