OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis

被引：2719

作者：

Kong, YY

Yoshida, H

Sarosi, I

Tan, HL

Timms, E

Capparelli, C

Morony, S

Oliveira-dos-Santos, AJ

Van, G

Itie, A

Khoo, W

Wakeham, A

Dunstan, CR

Lacey, DL

Mak, TW

Boyle, WJ

Penninger, JM

机构：

[1] Ontario Canc Inst, Amgen Inst, Toronto, ON M5G 2C1, Canada

[2] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2C1, Canada

[3] Univ Toronto, Dept Immunol, Toronto, ON M5G 2C1, Canada

[4] Amgen Inc, Dept Pathol, Thousand Oaks, CA 91320 USA

[5] Amgen Inc, Dept Cell Biol, Thousand Oaks, CA 91320 USA

来源：

NATURE | 1999年 / 397卷 / 6717期

关键词：

D O I：

10.1038/16852

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and Cop) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph-node organogenesis and lymphocyte development and Is an essential osteoclast differentiation factor in vivo

引用

页码：315 / 323

页数：9

共 50 条

[1] Generation of CD1(+)RelB(+) dendritic cells and tartrate-resistant acid phosphatase-positive osteoclast-like multinucleated giant cells from human monocytes [J].