Osteoimmunology
Osteoimmunology
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DOI：
10.1007/s00223-018-0421-5
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发表时间：
2018-04
影响因子：
4.2
通讯作者：
Stuart H. Ralston;G. Schett
中科院分区：
文献类型：
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作者：
Stuart H. Ralston;G. Schett
35年前，随着Horton的发现，免疫系统和骨骼之间的相互作用最初被认识到，激活的外周血白细胞释放一种可溶性的活性，刺激破骨细胞性骨吸收[1]。随着细胞和分子生物学的进步，自那以后发现了几个分子，它们在骨重建和免疫反应的调节中发挥作用，最著名的是核因子kappa B受体激活剂(RANK)和RANKL(RANKL)，它们最初被确定为T细胞激活和树突状细胞功能的介体[2]，但后来被发现是破骨细胞生成的关键调节因子[3]。大约18年前，Arron和Choi[4]首次创造了“骨免疫学”这个术语，用来描述骨细胞和免疫细胞相互作用的过程，当时Takayanagi在一篇精液论文中发表评论，表明RANKL诱导的T细胞对破骨细胞的激活被相同细胞产生的干扰素伽马抵消[5]。从这些开始，人们对骨免疫学学科的兴趣迅速发展(图1)。正是出于这个原因，我们在本期《钙化组织国际》上专门讨论了骨免疫学的话题。本期从Terashima和Takayanagi对该领域的权威和精美插图概述开始[6]。这篇综述来自该领域的领先实验室之一，详细介绍了RANKL用于调节破骨细胞生成的信号通路，并考虑了RANK-RANKL通路作为全身性骨丢失和伴随T细胞的局部骨丢失的媒介所起的作用
Interactions between the immune system and bone were initially recognised more than 35 years ago with the discovery by Horton that activated peripheral blood leukocytes release a soluble activity that stimulates osteoclastic bone resorption [1]. With advances in cell and molecular biology, several molecules have since been discovered that play roles both in the regulation of bone remodelling and immune responses, most notably receptor activator of nuclear factor kappa B (RANK) and RANK Ligand (RANKL) which were initially identified as mediators of T-cell activation and dendritic cell function [2] but which then were found to be crucial regulators of osteoclastogenesis [3].The term “osteoimmunology” was first coined about 18 years ago by Arron and Choi [4] to describe the process whereby bone cells and immune cells interact when commenting on a seminal paper by Takayanagi which showed that RANKL-induced activation of osteoclasts by T-cells was counterbalanced by interferon gamma produced by the same cells [5]. Since these beginnings, interest in the discipline of osteoimmunology has evolved rapidly (Fig. 1). It is for this reason that we have devoted the current issue of Calcified Tissue International to the topic of osteoimmunology. The issue begins with an authoritative and beautifully illustrated overview of the field by Terashima and Takayanagi [6]. This review, from one of the leading laboratories in the field, details the signalling pathways used by RANKL to regulate osteoclastogenesis and considers the role of the RANK–RANKL pathway as a mediator of both systemic bone loss and the local bone loss that accompanies T-cell