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关节炎相关的破骨细胞生成巨噬细胞(AtoM),是病理性骨侵蚀的关键因素。

Arthritis-associated osteoclastogenic macrophage, AtoM, as a key player in pathological bone erosion.

作者信息

Agemura Tomoya, Hasegawa Tetsuo, Yari Shinya, Kikuta Junichi, Ishii Masaru

机构信息

Department of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

WPI-Immunology Frontier Research Center, Osaka University, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.

出版信息

Inflamm Regen. 2022 Jun 2;42(1):17. doi: 10.1186/s41232-022-00206-w.

DOI:10.1186/s41232-022-00206-w
PMID:35650653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9161570/
Abstract

Osteoclasts are myeloid lineage cells with a unique bone-destroying ability that maintains bone homeostasis together with bone formation by osteoblasts. An advanced intravital imaging system using a two-photon microscopy has enabled the observation and evaluation of osteoclast dynamics and behaviors in the bone marrow of living mice. Using this system, it has become clear that pathological osteoclasts under inflamed conditions differ from physiological osteoclasts under a steady-state. Recently, we identified novel osteoclast precursors in arthritis, called arthritis-associated osteoclastogenic macrophages (AtoMs), which differentiate into pathological osteoclasts and induce inflammatory bone destruction. In this review, we introduce the in vivo imaging of physiological and pathological osteoclasts and their differentiation mechanism.

摘要

破骨细胞是具有独特骨破坏能力的髓系谱系细胞,它与成骨细胞的骨形成一起维持骨稳态。一种使用双光子显微镜的先进活体成像系统能够观察和评估活小鼠骨髓中破骨细胞的动态和行为。利用该系统,已经明确炎症条件下的病理性破骨细胞与稳态下的生理性破骨细胞不同。最近,我们在关节炎中鉴定出了新的破骨细胞前体,称为关节炎相关破骨细胞生成巨噬细胞(AtoMs),它们分化为病理性破骨细胞并诱导炎性骨破坏。在这篇综述中,我们介绍生理性和病理性破骨细胞的体内成像及其分化机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/6797b0614ad8/41232_2022_206_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/329aefc15a05/41232_2022_206_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/b76f06493daa/41232_2022_206_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/38c5187b4431/41232_2022_206_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/6797b0614ad8/41232_2022_206_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/329aefc15a05/41232_2022_206_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/b76f06493daa/41232_2022_206_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/38c5187b4431/41232_2022_206_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378d/9161570/6797b0614ad8/41232_2022_206_Fig4_HTML.jpg

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本文引用的文献

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Development of an intravital imaging system for the synovial tissue reveals the dynamics of CTLA-4 Ig in vivo.
开发一种用于滑膜组织的活体成像系统,揭示 CTLA-4Ig 在体内的动态变化。
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Identification of a novel arthritis-associated osteoclast precursor macrophage regulated by FoxM1.鉴定由 FoxM1 调控的新型关节炎相关破骨细胞前体细胞巨噬细胞。
Nat Immunol. 2019 Dec;20(12):1631-1643. doi: 10.1038/s41590-019-0526-7. Epub 2019 Nov 18.
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Locally renewing resident synovial macrophages provide a protective barrier for the joint.局部更新的驻留滑膜巨噬细胞为关节提供了一个保护屏障。
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Direct cell-cell contact between mature osteoblasts and osteoclasts dynamically controls their functions in vivo.成熟成骨细胞与破骨细胞之间的直接细胞间接触在体内动态控制它们的功能。
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