School of Dental Sciences and Institute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, UK.
J Clin Periodontol. 2011 Mar;38 Suppl 11:60-84. doi: 10.1111/j.1600-051X.2010.01671.x.
To review current knowledge on cytokine interactions and the cytokine-mediated links between innate and adaptive immunity that are relevant to the pathophysiology of periodontitis.
A structured review of the literature was undertaken to identify relevant research publications using a Medline search from 1950 to September 2010. The focus of the search was on the functional role of cytokines, i.e. their actions and responses relevant to the pathogenesis of periodontal disease rather than more descriptive studies of their expression in tissues and body fluids. It was not possible to conduct a traditional systematic review with a focussed question due to the heterogeneity of published research.
There is enormous heterogeneity in the periodontal literature in terms of experimental approaches. We have the deepest understanding of the role of the pro-inflammatory cytokines [e.g. interleukin (IL)-1β, tumour necrosis factor-α, IL-6] with accumulating data on T-cell regulatory cytokines (e.g. IL-12, IL-18), chemokines and cytokines which mediate bone cell development and function (e.g. receptor activator of NF-κB ligand, osteoprotegerin). It is clear that there are multiple, overlapping and complex functional links between cytokines with regulatory control exerted at a number of levels and involving numerous cell types (both immune cells and resident cells in the periodontium).
Cytokines appear to interact functionally in networks in the periodontium and integrate aspects of innate and adaptive immunity. However, our understanding is far from complete, particularly how molecular and cellular pathways relate to disease pathogenesis. We should adopt consistent experimental approaches to gain better insight into the totality of cytokine networks and how they drive immune responses in the periodontium.
回顾细胞因子相互作用以及固有免疫和适应性免疫之间细胞因子介导的联系的现有知识,这些知识与牙周炎的病理生理学有关。
通过 Medline 搜索,从 1950 年到 2010 年 9 月,对文献进行了系统的回顾,以确定相关的研究出版物。搜索的重点是细胞因子的功能作用,即它们与牙周病发病机制相关的作用和反应,而不是更具描述性的组织和体液中细胞因子表达的研究。由于发表研究的异质性,不可能提出一个具有重点问题的传统系统评价。
在实验方法方面,牙周文献存在巨大的异质性。我们对促炎细胞因子(例如白细胞介素 [IL]-1β、肿瘤坏死因子-α、IL-6)的作用有了更深入的了解,并且有越来越多的数据表明 T 细胞调节细胞因子(例如 IL-12、IL-18)、趋化因子和细胞因子调节骨细胞发育和功能(例如 NF-κB 配体受体激活剂、骨保护素)。显然,细胞因子之间存在多种重叠和复杂的功能联系,调节控制在多个水平上发挥作用,涉及许多细胞类型(包括免疫细胞和牙周组织中的固有细胞)。
细胞因子在牙周组织中似乎以功能网络的形式相互作用,并整合了固有免疫和适应性免疫的各个方面。然而,我们的理解还远远不够,特别是分子和细胞途径与疾病发病机制的关系。我们应该采用一致的实验方法,以更好地了解细胞因子网络的整体情况以及它们如何在牙周组织中驱动免疫反应。