[破骨细胞分化与激活]
[Osteoclast differentiation and activation].
作者信息
Takayanagi Hiroshi
机构信息
Tokyo Medical and Dental University, Graduate School, Department of Cell Signaling.
出版信息
Clin Calcium. 2007 Apr;17(4):484-92.
PMID:17404476
Abstract
In autoimmune arthritis, activation of T cells induces bone destruction through receptor activator of NF-kappaB ligand (RANKL) . Recent study revealed interleukin-17 (IL-17) -producing helper T cell subset (Th17) , but not IFN-gamma-producing Th1, to be responsible for bone destruction. Here we summarize the current understanding of osteoclast differentiation and activation in the context of osteoimmunology.
摘要
在自身免疫性关节炎中，T细胞的激活通过核因子κB受体激活剂配体（RANKL）诱导骨质破坏。最近的研究表明，产生白细胞介素-17（IL-17）的辅助性T细胞亚群（Th17）而非产生干扰素-γ的Th1细胞，是骨质破坏的原因。在此，我们总结了在骨免疫学背景下对破骨细胞分化和激活的当前认识。
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