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本文引用的文献

1
Osteoclastogenesis in peripheral blood mononuclear cell cultures of periprosthetic osteolysis patients and the phenotype of T cells localized in periprosthetic tissues.假体周围骨溶解患者外周血单个核细胞培养中的破骨细胞生成及假体周围组织中 T 细胞的表型。
Biomaterials. 2010 Oct;31(29):7519-25. doi: 10.1016/j.biomaterials.2010.06.027. Epub 2010 Jul 17.
2
MHC class II transactivator negatively regulates RANKL-mediated osteoclast differentiation by downregulating NFATc1 and OSCAR.MHC 类 II 转录激活因子通过下调 NFATc1 和 OSCAR 负调控 RANKL 介导的破骨细胞分化。
Cell Signal. 2010 Sep;22(9):1341-9. doi: 10.1016/j.cellsig.2010.05.001. Epub 2010 May 11.
3
CD16 (FcRgammaIII) as a potential marker of osteoclast precursors in psoriatic arthritis.CD16(FcRγIII)作为银屑病关节炎破骨细胞前体细胞的潜在标志物。
Arthritis Res Ther. 2010;12(1):R14. doi: 10.1186/ar2915. Epub 2010 Jan 26.
4
A novel T cell cytokine, secreted osteoclastogenic factor of activated T cells, induces osteoclast formation in a RANKL-independent manner.一种新型T细胞细胞因子,即活化T细胞分泌的破骨细胞生成因子,以一种不依赖RANKL的方式诱导破骨细胞形成。
Arthritis Rheum. 2009 Nov;60(11):3324-35. doi: 10.1002/art.24877.
5
Dendritic cells: a new player in osteoimmunology.树突状细胞:骨免疫学的新角色。
Curr Mol Med. 2009 Sep;9(7):893-910. doi: 10.2174/156652409789105507.
6
Expression of receptor activator of nuclear factor-kappaB ligand by B cells in response to oral bacteria.B细胞对口腔细菌的反应中核因子κB受体激活剂配体的表达
Oral Microbiol Immunol. 2009 Jun;24(3):190-6. doi: 10.1111/j.1399-302X.2008.00494.x.
7
Cross-presentation by osteoclasts induces FoxP3 in CD8+ T cells.破骨细胞的交叉呈递可诱导CD8+ T细胞中的FoxP3。
J Immunol. 2009 May 1;182(9):5477-87. doi: 10.4049/jimmunol.0803897.
8
CD137L- and RANKL-mediated reverse signals inhibit osteoclastogenesis and T lymphocyte proliferation.CD137L和RANKL介导的反向信号抑制破骨细胞生成和T淋巴细胞增殖。
Immunobiology. 2009;214(2):153-61. doi: 10.1016/j.imbio.2008.05.001. Epub 2008 Jun 26.
9
Alpha1beta1 integrin and interleukin-7 receptor up-regulate the expression of RANKL in human T cells and enhance their osteoclastogenic function.α1β1整合素和白细胞介素-7受体上调人T细胞中RANKL的表达并增强其破骨细胞生成功能。
Immunology. 2008 Nov;125(3):359-69. doi: 10.1111/j.1365-2567.2008.02858.x. Epub 2008 May 13.
10
Estrogen deficiency increases osteoclastogenesis up-regulating T cells activity: a key mechanism in osteoporosis.雌激素缺乏通过上调T细胞活性增加破骨细胞生成:骨质疏松症的关键机制。
Bone. 2008 Jul;43(1):92-100. doi: 10.1016/j.bone.2008.02.017. Epub 2008 Mar 7.

免疫系统与骨骼之间的相互作用。

Interactions between the immune system and bone.

作者信息

D'Amelio Patrizia, Fornelli Giorgia, Roato Ilaria, Isaia Giovanni Carlo

机构信息

Patrizia D'Amelio, Giorgia Fornelli, Giovanni Carlo Isaia, Department of Surgical and Medical Disciplines, Section of Gerontology, University of Torino, 10126 Torino, Italy.

出版信息

World J Orthop. 2011 Mar 18;2(3):25-30. doi: 10.5312/wjo.v2.i3.25.

DOI:10.5312/wjo.v2.i3.25
PMID:22474632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3302038/
Abstract

The relationship between the immune system, estrogen deficiency and bone loss is an intriguing and, as yet, unexplained challenge of the past two decades. Here we summarize the evidence that links immune cells, inflammation, cytokine production and osteoclast formation and activity with particular regard to humans.

摘要

免疫系统、雌激素缺乏与骨质流失之间的关系是过去二十年来一个引人关注但尚未得到解释的难题。在此,我们总结了将免疫细胞、炎症、细胞因子产生以及破骨细胞形成和活性联系起来的证据,尤其侧重于人类方面。