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[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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