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2
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本文引用的文献

1
Precise standardization of reagents for complement fixation.补体结合反应试剂的精确标准化
Am J Trop Med Hyg. 1963 Jan;12:103-16. doi: 10.4269/ajtmh.1963.12.103.
2
1958 REVISION of diagnostic criteria for rheumatoid arthritis.1958年类风湿性关节炎诊断标准修订版。
Arthritis Rheum. 1959 Feb;2(1):16-20. doi: 10.1002/1529-0131(195902)2:1<16::aid-art1780020104>3.0.co;2-9.
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Purification and radiolabeling of human C1q.人C1q的纯化与放射性标记
J Immunol. 1981 Aug;127(2):648-53.
4
Modulation of C2 biosynthesis by antigen-antibody complexes.抗原-抗体复合物对C2生物合成的调节作用。
J Clin Lab Immunol. 1982 Jan;7(1):15-9.
5
The proteolytic activation systems of complement.补体的蛋白水解激活系统。
Annu Rev Biochem. 1981;50:433-64. doi: 10.1146/annurev.bi.50.070181.002245.
6
Complement-mediated inhibition of immune precipitation. I. Role of the classical and alternative pathways.补体介导的免疫沉淀抑制作用。I. 经典途径和替代途径的作用
Clin Exp Immunol. 1982 Mar;47(3):555-62.
7
A comparison of the effects of heat-aggregated and chemically cross-linked IgG on monocyte C2 production.热聚集和化学交联IgG对单核细胞C2产生影响的比较。
Immunology. 1983 Jul;49(3):457-61.
8
Inhibition of immune precipitation by complement.补体对免疫沉淀的抑制作用。
Clin Exp Immunol. 1980 Nov;42(2):387-94.
9
IgM-RF prevents complement-mediated inhibition of immune precipitation.IgM类风湿因子可防止补体介导的免疫沉淀抑制作用。
Immunology. 1984 Jul;52(3):445-8.
10
Reduced complement-mediated immune complex solubilizing capacity and the presence of incompletely solubilized immune complexes in SLE sera.系统性红斑狼疮患者血清中补体介导的免疫复合物溶解能力降低以及存在未完全溶解的免疫复合物。
Clin Exp Immunol. 1983 Nov;54(2):439-47.

补体介导的免疫沉淀抑制因子的作用机制

Mechanism of action of an inhibitor of complement-mediated prevention of immune precipitation.

作者信息

Ahmed A E, Veitch J, Whaley K

机构信息

University of Glasgow, Department of Pathology, Western Infirmary, U.K.

出版信息

Immunology. 1990 Jun;70(2):139-44.

PMID:2373514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1384183/
Abstract

Glycoprotein 60 (gp60) is a normal plasma protein (mean concentration in normal serum 34 micrograms/ml) that is present in increased levels (mean concentration 97 micrograms/ml) in the sera of patients with rheumatoid arthritis (RA). Purified gp60 binds to IgG but not to IgM, and competitively inhibits the binding of C1q. In fluid-phase studies, purified gp60 was shown to reduce immune complex-mediated complement activation in a dose-dependent manner. The addition of Fab anti-gp60 to normal serum was associated with (i) increased levels of complement-mediated prevention of immune precipitation (PIP); (ii) increased total haemolytic complement activity when EAIgG, but not when EAIgM, were used as targets; and (iii) increased immune complex-mediated complement activation. Thus gp60 appears to regulate immune complex-mediated classical pathway activation. The findings that Fab anti-gp60 (i) only partly restored PIP in RA sera showing reduced PIP levels and (ii) only partly reduced inhibition of PIP by RA sera, show that gp60 is not entirely responsible for these abnormalities.

摘要

糖蛋白60(gp60)是一种正常的血浆蛋白(正常血清中的平均浓度为34微克/毫升),在类风湿性关节炎(RA)患者的血清中水平升高(平均浓度为97微克/毫升)。纯化的gp60与IgG结合,但不与IgM结合,并竞争性抑制C1q的结合。在液相研究中,纯化的gp60被证明以剂量依赖的方式减少免疫复合物介导的补体激活。向正常血清中添加抗gp60 Fab与以下情况相关:(i)补体介导的免疫沉淀预防(PIP)水平增加;(ii)当以EA IgG而非EA IgM作为靶标时,总溶血补体活性增加;(iii)免疫复合物介导的补体激活增加。因此,gp60似乎调节免疫复合物介导的经典途径激活。抗gp60 Fab(i)仅部分恢复了PIP水平降低的RA血清中的PIP,以及(ii)仅部分降低了RA血清对PIP的抑制作用,这些发现表明gp60并非完全导致这些异常。