• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

巨噬细胞在慢性关节炎中的作用。

The role of macrophages in chronic arthritis.

作者信息

van den Berg W B, van Lent P L

机构信息

Department of Rheumatology, University Hospital Nijmegen, The Netherlands.

出版信息

Immunobiology. 1996 Oct;195(4-5):614-23. doi: 10.1016/S0171-2985(96)80026-X.

DOI:10.1016/S0171-2985(96)80026-X
PMID:8933161
Abstract

Rheumatoid arthritis is characterized by a mononuclear infiltrate in the synovial tissue of the affected joints, considerable thickening of the synovial lining layer and concomitant destruction of cartilage and bone. Macrophages probably play a central role and the contribution of the synovial lining macrophages is addressed in studies in experimental murine arthritis models. Emphasis is given to the involvement in arthritis expression and cartilage destruction. The role of TNF-alpha and IL-1, and the modulatory cytokines IL-4/ IL-10 is briefly discussed.

摘要

类风湿性关节炎的特征是受累关节的滑膜组织中有单核细胞浸润、滑膜衬里层显著增厚以及伴随的软骨和骨破坏。巨噬细胞可能起核心作用,滑膜衬里巨噬细胞的作用在实验性小鼠关节炎模型研究中得到探讨。重点是其在关节炎表现和软骨破坏中的作用。简要讨论了肿瘤坏死因子-α和白细胞介素-1以及调节性细胞因子白细胞介素-4/白细胞介素-10的作用。

相似文献

1
The role of macrophages in chronic arthritis.巨噬细胞在慢性关节炎中的作用。
Immunobiology. 1996 Oct;195(4-5):614-23. doi: 10.1016/S0171-2985(96)80026-X.
2
Elevated expression of interleukin-7 receptor in inflamed joints mediates interleukin-7-induced immune activation in rheumatoid arthritis.炎症关节中白细胞介素-7受体的表达升高介导类风湿关节炎中白细胞介素-7诱导的免疫激活。
Arthritis Rheum. 2009 Sep;60(9):2595-605. doi: 10.1002/art.24754.
3
LILRA5 is expressed by synovial tissue macrophages in rheumatoid arthritis, selectively induces pro-inflammatory cytokines and IL-10 and is regulated by TNF-alpha, IL-10 and IFN-gamma.LILRA5在类风湿性关节炎中由滑膜组织巨噬细胞表达,选择性诱导促炎细胞因子和白细胞介素-10,并受肿瘤坏死因子-α、白细胞介素-10和干扰素-γ调节。
Eur J Immunol. 2008 Dec;38(12):3459-73. doi: 10.1002/eji.200838415.
4
Fc gamma R expression on macrophages is related to severity and chronicity of synovial inflammation and cartilage destruction during experimental immune-complex-mediated arthritis (ICA).巨噬细胞上FcγR的表达与实验性免疫复合物介导的关节炎(ICA)期间滑膜炎症和软骨破坏的严重程度及慢性程度相关。
Arthritis Res. 2000;2(6):489-503. doi: 10.1186/ar131. Epub 2000 Aug 31.
5
Expression of Toll-like receptor 2 on CD16+ blood monocytes and synovial tissue macrophages in rheumatoid arthritis.类风湿关节炎中CD16⁺血液单核细胞和滑膜组织巨噬细胞上Toll样受体2的表达
Arthritis Rheum. 2004 May;50(5):1457-67. doi: 10.1002/art.20219.
6
[Quantification of macrophages and granulocytes at the joint cartilage-pannus junction in rheumatoid arthritis].[类风湿关节炎中关节软骨-血管翳交界处巨噬细胞和粒细胞的定量分析]
Z Rheumatol. 1996 Nov-Dec;55(6):401-9.
7
Phagocytic synovial lining cells regulate acute and chronic joint inflammation after antigenic exacerbation of smouldering experimental murine arthritis.吞噬性滑膜衬里细胞在隐匿性实验性小鼠关节炎抗原性加重后调节急性和慢性关节炎症。
J Rheumatol. 1998 Jun;25(6):1135-45.
8
Dysregulation of interleukin-10-dependent gene expression in rheumatoid arthritis synovial macrophages.类风湿性关节炎滑膜巨噬细胞中白细胞介素-10依赖性基因表达的失调。
Arthritis Rheum. 2006 Sep;54(9):2711-21. doi: 10.1002/art.22055.
9
LIGHT is involved in the pathogenesis of rheumatoid arthritis by inducing the expression of pro-inflammatory cytokines and MMP-9 in macrophages.LIGHT通过诱导巨噬细胞中促炎细胞因子和MMP-9的表达参与类风湿性关节炎的发病机制。
Immunology. 2005 Feb;114(2):272-9. doi: 10.1111/j.1365-2567.2004.02004.x.
10
Mechanism of joint destruction in rheumatoid arthritis.类风湿关节炎中关节破坏的机制。
Arch Immunol Ther Exp (Warsz). 1998;46(1):1-7.

引用本文的文献

1
A Mendelian randomization study of the gut microbiota and risk of knee osteoarthritis and the mediating role of immune cells.肠道微生物群与膝关节骨关节炎风险的孟德尔随机化研究及免疫细胞的中介作用。
Sci Rep. 2025 Aug 4;15(1):28455. doi: 10.1038/s41598-025-14007-x.
2
β-Sitosterol modulates macrophage polarization and attenuates rheumatoid inflammation in mice.β-谷甾醇调节巨噬细胞极化,减轻小鼠类风湿性炎症。
Pharm Biol. 2019 Dec;57(1):161-168. doi: 10.1080/13880209.2019.1577461.
3
The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.
吞噬细胞凋亡途径在风湿性疾病中的炎症作用。
Nat Rev Rheumatol. 2016 Aug 23;12(9):543-58. doi: 10.1038/nrrheum.2016.132.
4
Targeted drug-delivery approaches by nanoparticulate carriers in the therapy of inflammatory diseases.纳米颗粒载体靶向递药治疗炎症性疾病。
J R Soc Interface. 2010 Feb 6;7 Suppl 1(Suppl 1):S55-66. doi: 10.1098/rsif.2009.0285.focus. Epub 2009 Nov 25.
5
Photodynamic therapy using talaporfin sodium for synovial membrane from rheumatoid arthritis patients and collagen-induced arthritis rats.使用替拉泊芬钠对类风湿性关节炎患者和胶原诱导性关节炎大鼠的滑膜进行光动力治疗。
Clin Rheumatol. 2008 Jun;27(6):751-61. doi: 10.1007/s10067-007-0794-8. Epub 2007 Dec 8.
6
Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis.促凋亡蛋白Bid对于炎症性关节炎效应期的消退是必需的。
Arthritis Res Ther. 2007;9(3):R49. doi: 10.1186/ar2204.
7
Circulating levels of the chemokine CCL18 but not CXCL16 are elevated and correlate with disease activity in rheumatoid arthritis.趋化因子CCL18而非CXCL16的循环水平在类风湿性关节炎中升高,并与疾病活动相关。
Ann Rheum Dis. 2007 Oct;66(10):1334-8. doi: 10.1136/ard.2006.066084. Epub 2007 Mar 9.
8
Novel insights in the regulation of CCL18 secretion by monocytes and dendritic cells via cytokines, toll-like receptors and rheumatoid synovial fluid.单核细胞和树突状细胞通过细胞因子、Toll样受体和类风湿性滑液调节CCL18分泌的新见解。
BMC Immunol. 2006 Sep 19;7:23. doi: 10.1186/1471-2172-7-23.
9
p21Cip1 is required for the development of monocytes and their response to serum transfer-induced arthritis.p21Cip1是单核细胞发育及其对血清转移诱导性关节炎反应所必需的。
Am J Pathol. 2006 May;168(5):1531-41. doi: 10.2353/ajpath.2006.050555.
10
Immune complexes from rheumatoid arthritis synovial fluid induce FcgammaRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-alpha by peripheral blood mononuclear cells.类风湿性关节炎滑液中的免疫复合物可诱导外周血单核细胞产生肿瘤坏死因子-α,此过程依赖FcγRIIa且与类风湿因子相关。
Arthritis Res Ther. 2006;8(3):R64. doi: 10.1186/ar1926. Epub 2006 Mar 28.