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慢性溶骨性疾病中的巨噬细胞免疫调节——以牙周炎为例。

Macrophage immunomodulation in chronic osteolytic diseases-the case of periodontitis.

机构信息

Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Harvard Medical School, Boston, Massachusetts, USA.

Dental Research Institute, Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada.

出版信息

J Leukoc Biol. 2019 Mar;105(3):473-487. doi: 10.1002/JLB.1RU0818-310R. Epub 2018 Nov 19.

DOI:10.1002/JLB.1RU0818-310R
PMID:30452781
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6386606/
Abstract

Periodontitis (PD) is a chronic osteolytic disease that shares pathogenic inflammatory features with other conditions associated with nonresolving inflammation. A hallmark of PD is inflammation-mediated alveolar bone loss. Myeloid cells, in particular polymorphonuclear neutrophils (PMN) and macrophages (Mac), are essential players in PD by control of gingival biofilm pathogenicity, activation of adaptive immunity, as well as nonresolving inflammation and collateral tissue damage. Despite mounting evidence of significant innate immune implications to PD progression and healing after therapy, myeloid cell markers and targets for immune modulation have not been validated for clinical use. The remarkable plasticity of monocytes/Mac in response to local activation factors enables these cells to play central roles in inflammation and restoration of tissue homeostasis and provides opportunities for biomarker and therapeutic target discovery for management of chronic inflammatory conditions, including osteolytic diseases such as PD and arthritis. Along a wide spectrum of activation states ranging from proinflammatory to pro-resolving, Macs respond to environmental changes in a site-specific manner in virtually all tissues. This review summarizes the existing evidence on Mac immunomodulation therapies for osteolytic diseases in the broader context of conditions associated with nonresolving inflammation, and discusses osteoimmune implications of Macs in PD.

摘要

牙周炎(PD)是一种慢性溶骨性疾病,其具有与其他与非解决炎症相关的疾病的致病炎症特征。PD 的一个标志是炎症介导的牙槽骨丧失。髓样细胞,特别是多形核中性粒细胞(PMN)和巨噬细胞(Mac),通过控制牙龈生物膜的致病性、激活适应性免疫以及非解决炎症和附带组织损伤,是 PD 的重要参与者。尽管有大量证据表明先天免疫对 PD 进展和治疗后愈合有重要影响,但髓样细胞标志物和免疫调节靶点尚未得到临床验证。单核细胞/巨噬细胞对局部激活因子的显著可塑性使这些细胞在炎症和组织稳态的恢复中发挥核心作用,并为慢性炎症性疾病(包括溶骨性疾病如 PD 和关节炎)的生物标志物和治疗靶点的发现提供了机会。巨噬细胞在从促炎到抗炎的广泛激活状态范围内,以特定于部位的方式对环境变化作出反应,几乎存在于所有组织中。本文综述了在与非解决炎症相关的条件的更广泛背景下,针对溶骨性疾病的巨噬细胞免疫调节治疗的现有证据,并讨论了巨噬细胞在 PD 中的骨免疫影响。

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Emergence of immunoregulatory Ym1Ly6C monocytes during recovery phase of tissue injury.组织损伤恢复阶段免疫调节性 Ym1Ly6C 单核细胞的出现。
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Mechanism of fibrosis inhibition in laser induced choroidal neovascularization by doxycycline.多西环素抑制激光诱导脉络膜新生血管纤维化的机制。
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Fibroblast derived C3 promotes the progression of experimental periodontitis through macrophage M1 polarization and osteoclast differentiation.成纤维细胞衍生的C3通过巨噬细胞M1极化和破骨细胞分化促进实验性牙周炎的进展。
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