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首页> 外文期刊>Current opinion in gastroenterology >The pathophysiologic rationale for biological therapies in inflammatory bowel disease.
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The pathophysiologic rationale for biological therapies in inflammatory bowel disease.

机译：炎症性肠病的生物疗法的病理生理原理。

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PURPOSE OF REVIEW: Inflammatory bowel disease is driven by an excessive immune response in the gut wall. This review summarises important new developments in understanding this immune response and the downstream mechanisms of intestinal injury, alongside their potential role in opening up new avenues of treatment. RECENT FINDINGS: The evidence continues to accumulate that Crohn's disease is primarily due to a T helper cell-type 1 immune response in the gut wall. IL-12 and IL-18 appear to be the cytokines primarily responsible for Th1 polarisation, but IL-21 may also be important. The p40 chain of IL-12 also associates with a novel p19 chain to form IL-23 which is also a potent Th1-inducing cytokine but the expression of IL-23 in Crohn's disease has not been reported. Progress in understanding the immunology of ulcerative colitis remains slow, but IL-13 produced by natural killer T cells may be involved. T-cell resistance to apoptosis occurs in Crohn's disease, and human and mouse studies indicate that the signalling molecule STAT3, which transduces signals from IL-6 and IL-10, is involved in mucosal T cell homeostasis. Fibroblasts and metalloproteinases continue be implicated in ulceration, fibrosis, and fistula formation. SUMMARY: Understanding the immunology of inflammatory bowel disease continues to underpin the vast majority of new therapies and identifies new targets. Novel approaches, such as exploiting the antiinflammatory role of cannabinoid receptors, may also prove productive in the future.
机译：审查目的：肠壁过度的免疫反应可引起炎症性肠病。这篇综述总结了在理解这种免疫反应和肠损伤下游机制方面的重要新进展，以及它们在开辟新治疗途径方面的潜在作用。最近的发现：证据不断积累，克罗恩氏病主要是由于肠壁中的T辅助细胞1型免疫应答引起的。 IL-12和IL-18似乎是主要引起Th1极化的细胞因子，但IL-21也可能很重要。 IL-12的p40链也与新的p19链结合形成IL-23，IL-23也是有效的Th1诱导细胞因子，但尚未报道克罗恩病中IL-23的表达。溃疡性结肠炎的免疫学研究进展仍然缓慢，但自然杀伤性T细胞产生的IL-13可能参与其中。 T细胞对细胞凋亡的抗性在克罗恩病中发生，人类和小鼠研究表明，信号分子STAT3可以转导来自IL-6和IL-10的信号，参与粘膜T细胞稳态。成纤维细胞和金属蛋白酶继续与溃疡，纤维化和瘘管形成有关。摘要：了解炎症性肠病的免疫学继续为绝大多数新疗法奠定基础并确定新的靶标。诸如开发大麻素受体的抗炎作用等新方法在将来也可能会产生成果。

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