欢迎访问《现代生物医学进展》编辑部！

炎症性肠病(Inflammatory Bowel Diseases, IBD)，是一组病因未明的累及胃肠道的慢性炎症性疾病，一般指克罗恩病(Crohn's disease, CD)和溃疡性结肠炎(ulcerative colitis, UC)。目前认为它是由多种因素相互作用所致的一种自身免疫性疾病，主要包括免疫、环境以及遗传等因素，其中免疫在IBD 的发生过程中起着极其重要的作用。以往研究认为与T 辅助细胞（T Helper cells）Th1 或Th2 细胞反应的增强或减弱有关。然而最近研究发现一类新细胞亚群, 称为Th17 细胞，与之相关的细胞因子可导致包括肠道在内的多脏器病变。Th17 细胞分化过程中又需要IL-23 的参与，因此IL-23/Th17 细胞在炎症性肠病患者肠道内过度表达可以解释肠组织损伤的新途径，并为制定新的治疗策略提出依据。本文就IL-23/Th17 轴在炎症性肠病中的作用的研究进展作一综述。

英文摘要:

Crohn's disease (CD) and ulcerative colitis (UC) are the major forms of inflammatory bowel diseases (IBDs) in humans. The etiology of IBD is still unknown, but evidence has been accumulated to indicate that environmental and genetic factors contribute to promote an immunopathologic process leading to chronic inflammation. IBDs have been traditionally associated with exaggerated and poorly controlled T helper (Th) type 1 or Th2 cell response, respectively. More recent studies have, however, shown that IBDs are also characterized by a sustained production of cytokines made by a distinct lineage of Th cells, termed Th17 cells. The demonstration that Th17-related cytokines cause pathology in many organs, including the gut, and that expansion and maintenance of Th17 cell responses require the activity of IL-23, a cytokine made in excess in the gut of IBD patients has contributed to elucidate new pathways of intestinal tissue damage as well as to design new therapeutic strategies. In this review, we discuss the available data supporting the role of the IL-23/Th17 axis in themodulation of intestinal tissue inflammation.

View Full Text View/Add Comment Download reader