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From basic advances to therapeutic strategies in ulcerative colitis

机译:从溃疡性结肠炎的基本进展到治疗策略

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摘要

This is an exciting time for clinical and basic investigators in the field of inflammatory bowel disease. Previously considered unfashionable or impenetrable, ulcerative colitis (UC) and Crohn's disease are now attracting vigorous research attention with new technology being applied to hitherto insoluble questions. An example of the effective application of new technology in molecular biology to the study of inflammatory bowel disease is the recent generation of several genetically engineered rodent models that resemble UC.~(1,2) These animal models include enhanced expression (transgenic) or deletion (knockout) of specific genes coding for histocom-patibility antigens, cytokines, or T-cell receptor molecules. Such models enable current concepts of pathogenesis to be tested and new ones formulated. Lessons from these models include the demonstration that colitis can result from a primary defect in immune regulation, that more than one mechanism may be involved, and that mucosal T cells and their regulatory cytokines have a pivotal role in pathogenesis. The role of enteric microflora in the disease process has also been supported by the attenuation of mucosal inflammation when animals are bred in a germ-free environment.
机译:对于炎症性肠病领域的临床和基础研究人员来说,这是一个令人兴奋的时刻。溃疡性结肠炎(UC)和克罗恩氏病(Crohn's disease)以前被认为不合时宜或不可穿透,如今,由于将新技术应用于迄今无法解决的问题,溃疡性结肠炎(Crohn's disease)引起了研究的广泛关注。在分子生物学中有效应用新技术研究炎症性肠病的一个例子是最近几代类似于UC的基因工程啮齿动物模型。(1,2)这些动物模型包括增强的表达(转基因)或缺失(基因敲除)编码组织相容性抗原,细胞因子或T细胞受体分子的特定基因。这样的模型可以测试当前的发病机理,并制定新的发病机理。这些模型的经验教训表明,结肠炎可能是免疫调节的主要缺陷引起的,可能涉及多种机制,并且粘膜T细胞及其调节性细胞因子在发病机理中起着关键作用。当在无菌环境中饲养动物时,肠道菌群在疾病过程中的作用也得到了粘膜炎症减弱的支持。

著录项

  • 来源
    《Quarterly Journal of Medicine》 |1995年第9期|p.599-602|共4页
  • 作者

    F. Shanahan;

  • 作者单位

    Department of Medicine Cork University Hospital National University of Ireland Cork Ireland;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;临床医学;
  • 关键词

  • 入库时间 2022-08-18 00:54:21

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