期刊
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
卷 41, 期 12, 页码 1361-1366出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2362.2011.02545.x
关键词
Bone; cytokine; immunology; inflammation
资金
- German Research Council (DFG)
Background Inflammatory diseases are linked to enhanced bone loss. The effect of inflammation on bone is mediated by proinflammatory cytokines, which regulate bone formation as well as bone resorption thereby altering bone homeostasis. Materials and methods In this article we summarize the key insights in cytokine regulation of bone. We describe the major pro- and anti-inflammatory mediators, which are involved in the regulation of bone and describe the mechanisms by which these cytokines alter bone balance. Results We describe the effects of tumor necrosis factor (TNF), interleukin (IL)- 1 family members, IL-6, IL-17 and interferons (IFN) on bone and discuss the mechanisms by which these individual cytokines affect the bone resorbing and the bone forming cells. Conclusions Several proinflammatory cytokines (such as TNFa, IL-1 and IL-17) are major triggers for osteoclast activation explaining the enhanced bone loss during inflammation. Other such as IL-12, IL-18, IL-33 and IFN are strong suppressors of osteoclast differentiation and inhibit bone loss. Thus the cytokine composition of an inflammatory tissue is decisive whether inflammation triggers bone loss or not.
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