RANK-L AND RANK: T cells, bone loss, and mammalian evolution

被引:628
作者
Theill, LE
Boyle, WJ
Penninger, JM
机构
[1] Ontario Canc Inst, Amgen Inst, Toronto, ON M5G 2C1, Canada
[2] Amgen Inc, Inflammat Drug Discovery Res, Thousand Oaks, CA 91320 USA
[3] Amgen Inc, Discovery Res, Thousand Oaks, CA 91320 USA
[4] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2C1, Canada
[5] Univ Toronto, Dept Immunol, Toronto, ON M5G 2C1, Canada
关键词
T cell-dendritic cell interaction; osteoimmunology; TNF/TNFR super family molecules; osteoclast;
D O I
10.1146/annurev.immunol.20.100301.064753
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
TNF and TNFR family proteins play important roles in the control of cell death, proliferation, autoimmunity, the function of immune cells, or the organogenesis of lymphoid organs. Recently, novel members of this large family have been identified that have critical functions in immunity and that couple lymphoid cells with other organ systems such as bone morphogenesis and mammary gland formation in pregnancy. The TNF-family molecule RANK-L (RANK-L, TRANCE, ODF) and its receptor RANK are key regulators of bone remodeling, and they are essential for the development and activation of osteoclasts. Intriguingly, RANK-L/RANK interactions also regulate T cell/dendritic cell communications, dendritic cell survival, and lymph node formation; T cell-derived RANK-L can mediate bone loss in arthritis and periodontal disease. Moreover, RANK-L and RANK are expressed in mammary gland epithelial cells, and they control the development of a lactating mammary gland during pregnancy and the propagation of mammalian species. Modulation of these systems provides us with a unique opportunity to design novel therapeutics to inhibit bone loss in arthritis, periodontal disease, and osteoporosis.
引用
收藏
页码:795 / 823
页数:33
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