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1
Stimulation of human rheumatoid synovial cells by non-lethal complement membrane attack.非致死性补体膜攻击对人类风湿性滑膜细胞的刺激作用。
Immunology. 1990 Feb;69(2):237-42.
2
Human rheumatoid synovial cell stimulation by the membrane attack complex and other pore-forming toxins in vitro: the role of calcium in cell activation.膜攻击复合物及其他成孔毒素对人类风湿性滑膜细胞的体外刺激:钙在细胞活化中的作用
Immunology. 1990 Nov;71(3):312-6.
3
In vivo and in vitro evidence of cell recovery from complement attack in rheumatoid synovium.
Clin Exp Immunol. 1988 Sep;73(3):467-72.
4
Synthesis of interleukin 1beta, tumor necrosis factor-alpha, and interstitial collagenase (MMP-1) is eicosanoid dependent in human osteoarthritis synovial membrane explants: interactions with antiinflammatory cytokines.白细胞介素1β、肿瘤坏死因子-α和间质胶原酶(基质金属蛋白酶-1)的合成在人类骨关节炎滑膜组织外植体中依赖于类花生酸:与抗炎细胞因子的相互作用。
J Rheumatol. 2002 Mar;29(3):546-53.
5
Levels of SC5b--9 complement complex in plasma and synovial fluid of patients with rheumatic disease.风湿性疾病患者血浆和滑液中SC5b-9补体复合物的水平。
Med Interne. 1990 Oct-Dec;28(4):305-10.
6
Immunohistochemical determination of complement activation in joint tissues of patients with rheumatoid arthritis and osteoarthritis using neoantigen-specific monoclonal antibodies.使用新抗原特异性单克隆抗体对类风湿性关节炎和骨关节炎患者关节组织中的补体激活进行免疫组织化学测定。
J Clin Lab Immunol. 1992;37(4):147-62.
7
Measurement of terminal complement complexes in rheumatoid arthritis.类风湿关节炎中终末补体复合物的测定。
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8
Increasing production of matrix metalloproteinases, tumor necrosis factor-α, vascular endothelial growth factor and prostaglandin E2 in rheumatoid arthritis synovial fibroblasts by different adiponectin isoforms in a concentration-dependent manner.不同脂联素亚型以浓度依赖性方式增加类风湿性关节炎滑膜成纤维细胞中基质金属蛋白酶、肿瘤坏死因子-α、血管内皮生长因子和前列腺素E2的产生。
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Interaction of the terminal complement components C5b-9 with synovial fibroblasts: binding to the membrane surface leads to increased levels in collagenase-specific mRNA.补体终末成分C5b-9与滑膜成纤维细胞的相互作用:与膜表面结合导致胶原酶特异性mRNA水平升高。
Immunology. 1993 Feb;78(2):329-34.
10
Tumor necrosis factor alpha, a cytokine coregulating sugar uptake by cultured human synovial cells.肿瘤坏死因子α,一种调节培养的人滑膜细胞糖摄取的细胞因子。
Cell Biol Int. 1994 Mar;18(3):159-64. doi: 10.1006/cbir.1994.1056.

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Complement Attack against Aspergillus and Corresponding Evasion Mechanisms.针对曲霉的补体攻击及相应的逃避机制。
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Modulation of leukocyte recruitment and IL-8 expression by the membrane attack complex of complement (C5b-9) in a rabbit model of antigen-induced arthritis.在抗原诱导性关节炎兔模型中补体膜攻击复合物(C5b-9)对白细胞募集和IL-8表达的调节作用
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Urinary Tract Infection in Pregnant Women: Old Dogmas and Current Concepts Regarding Pathogenesis.
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8
Complement in acute and chronic arthritides: assessment of C3c, C9, and protectin (CD59) in synovial membrane.急性和慢性关节炎中的补体:滑膜中C3c、C9和膜攻击复合物抑制因子(CD59)的评估
Ann Rheum Dis. 1996 Dec;55(12):888-94. doi: 10.1136/ard.55.12.888.
9
Adhesion molecule expression and complement activation in vessel walls in synovial tissue from patients with chronic inflammatory joint disease.慢性炎症性关节病患者滑膜组织血管壁中黏附分子表达及补体激活情况
Clin Rheumatol. 1996 Sep;15(5):441-7. doi: 10.1007/BF02229640.
10
The membrane attack complex of complement induces interleukin-8 and monocyte chemoattractant protein-1 secretion from human umbilical vein endothelial cells.补体膜攻击复合物可诱导人脐静脉内皮细胞分泌白细胞介素-8和单核细胞趋化蛋白-1。
Am J Pathol. 1996 Sep;149(3):953-61.

本文引用的文献

1
Characterization of human complement components C6 and C7.人类补体成分C6和C7的特性分析
Mol Immunol. 1982 Nov;19(11):1425-31. doi: 10.1016/0161-5890(82)90189-4.
2
Identification of three major synovial lining cell populations by monoclonal antibodies directed to Ia antigens and antigens associated with monocytes/macrophages and fibroblasts.通过针对Ia抗原以及与单核细胞/巨噬细胞和成纤维细胞相关的抗原的单克隆抗体鉴定出三种主要的滑膜衬里细胞群。
Scand J Immunol. 1983 Jan;17(1):69-82. doi: 10.1111/j.1365-3083.1983.tb00767.x.
3
Stimulation by human interleukin 1 of cartilage breakdown and production of collagenase and proteoglycanase by human chondrocytes but not by human osteoblasts in vitro.在体外,人白细胞介素1刺激人软骨细胞导致软骨分解并产生胶原酶和蛋白聚糖酶,但不刺激人成骨细胞。
Biochim Biophys Acta. 1984 Feb 14;797(2):186-93. doi: 10.1016/0304-4165(84)90121-1.
4
Size of the transmembrane channels produced by complement proteins C5b-8.补体蛋白C5b - 8产生的跨膜通道的大小。
J Immunol. 1982 Sep;129(3):1143-6.
5
Immunoaffinity purification of human complement component C9 using monoclonal antibodies.使用单克隆抗体对人补体成分C9进行免疫亲和纯化。
J Immunol Methods. 1983 Nov 25;64(3):269-81. doi: 10.1016/0022-1759(83)90434-9.
6
Mechanism of cytolysis by complement.补体介导的细胞溶解机制。
Proc Natl Acad Sci U S A. 1972 Oct;69(10):2954-8. doi: 10.1073/pnas.69.10.2954.
7
IgG and IgM rheumatoid factor synthesis in rheumatoid synovial membrane cell cultures.类风湿性滑膜膜细胞培养物中IgG和IgM类风湿因子的合成
Arthritis Rheum. 1985 Jul;28(7):742-52. doi: 10.1002/art.1780280704.
8
Release of interleukin-1 from human synovial tissue in vitro.白细胞介素-1在人滑膜组织中的体外释放。
Arthritis Rheum. 1985 Aug;28(8):853-62. doi: 10.1002/art.1780280804.
9
Recovery of human neutrophils from complement attack: removal of the membrane attack complex by endocytosis and exocytosis.人中性粒细胞从补体攻击中恢复:通过内吞作用和胞吐作用去除膜攻击复合物。
J Immunol. 1987 Jan 1;138(1):246-53.
10
Membrane attack complex of complement in rheumatoid synovial tissue demonstrated by immunofluorescent microscopy.免疫荧光显微镜显示类风湿性滑膜组织中补体的膜攻击复合物。
J Rheumatol. 1986 Dec;13(6):1028-34.

非致死性补体膜攻击对人类风湿性滑膜细胞的刺激作用。

Stimulation of human rheumatoid synovial cells by non-lethal complement membrane attack.

作者信息

Daniels R H, Houston W A, Petersen M M, Williams J D, Williams B D, Morgan B P

机构信息

Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, U.K.

出版信息

Immunology. 1990 Feb;69(2):237-42.

PMID:2155179
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1385595/
Abstract

The effects of non-lethal complement attack on cultured human rheumatoid synovial cells have been investigated by measuring a variety of parameters. Within 3-4 min of initiating non-lethal complement membrane attack there was a rise in reactive oxygen metabolite release from cultured synovial cells, which slowly returned to basal levels over a period of 45 min. The response was dependent on the formation of the complete C5b-9 complex. Prostaglandin E2 was also released during non-lethal attack in a biphasic manner, an early phase of release occurring within the first hour and a second, larger phase commencing at 4 hr and rising to levels of over 1000 ng/10(6) cells at 24 hr, compared to control levels at this time of less than 100 ng/10(6) cells. This response was dependent on the formation of the C5b-8 complex but did not require C9. Removal of extracellular calcium reduced release of prostaglandin E2 to background levels, and inclusion of an inhibitor of protein synthesis abolished the second phase of release but not the first phase. Non-lethal attack caused release of small amounts of leukotriene B4 but no detectable release of tumour necrosis factor.

摘要

通过测量多种参数,研究了非致死性补体攻击对培养的人类风湿性滑膜细胞的影响。在启动非致死性补体膜攻击后的3 - 4分钟内,培养的滑膜细胞释放的活性氧代谢产物增加,在45分钟内缓慢恢复到基础水平。该反应依赖于完整的C5b - 9复合物的形成。前列腺素E2在非致死性攻击期间也以双相方式释放,早期释放发生在最初的一小时内,第二个更大的阶段在4小时开始,并在24小时时升至超过1000 ng/10(6)个细胞的水平,而此时对照水平低于100 ng/10(6)个细胞。该反应依赖于C5b - 8复合物的形成,但不需要C9。去除细胞外钙可将前列腺素E2的释放降低至背景水平,加入蛋白质合成抑制剂可消除第二阶段的释放,但不影响第一阶段。非致死性攻击导致少量白三烯B4的释放,但未检测到肿瘤坏死因子的释放。