期刊
IMMUNOLOGY
卷 155, 期 3, 页码 320-330出版社
WILEY
DOI: 10.1111/imm.12989
关键词
epithelial cell; inflammasome; inflammation
类别
资金
- Sir Henry Dale Fellowship - Wellcome Trust [104192/Z/14/Z]
- Sir Henry Dale Fellowship - Royal Society [104192/Z/14/Z]
- Manchester Collaborative Centre for Inflammation Research
- AstraZeneca
- GlaxoSmithKline
- University of Manchester
- Wellcome Trust [104192/Z/14/Z] Funding Source: Wellcome Trust
As a result of its strategic location, the epithelium is constantly exposed to a wide variety of pathogen and danger signals. Traditionally, the epithelium has been perceived as a defensive but passive barrier; however, it has now become evident that the epithelium senses and actively responds to these signals in order to maintain barrier homeostasis and contributes to the inflammatory response. One way it does this is by producing pro-inflammatory cytokines including interleukin-1 beta (IL-1 beta) and IL-18. These two cytokines are synthesized as inactive precursors, the maturation of which is mediated by pro-inflammatory caspases after the activation and assembly of macromolecular complexes called inflammasomes. Epithelial cells express a large panel of inflammasome components, and although the molecular mechanisms underlying the activation of these complexes in haematopoietic cells are well understood, how epithelial cells react to danger signals to activate the inflammasome remains unclear. We review and discuss how different inflammasomes contribute to barrier homeostasis and inflammation at several barrier sites, their mechanisms and how their aberrant regulation contributes to disease at the different epithelia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据