Membrane‐bound complement regulatory activity is decreased on vaccinia virus‐infected cells
Membrane‐bound complement regulatory activity is decreased on vaccinia virus‐infected cells
复制标题
痘苗病毒感染细胞的膜结合补体调节活性降低
DOI：
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发表时间：
1994
影响因子：
4.6
通讯作者：
H. Okada
中科院分区：
文献类型：
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作者：
L. Baranyi;N. Okada;K. Baranji;H. Takizawa;H. Okada
衰变加速因子（Decay Accelerating Factor，CRF）、膜辅因子蛋白（Membrane Cofactor Protein，MCP）、补体受体1和小鼠Crry是细胞表面结合的补体调节蛋白，能够抑制细胞膜上的C3转化酶活性，因此能够提供实质性保护，免受经典或旁路途径激活的同源补体的攻击。补体调节活性的降低可能导致自发性补体沉积和随后的细胞损伤。MoAb 512可抑制大鼠细胞上分子的补体调节活性，导致同源补体沉积。512单抗在大鼠体内识别的抗原与小鼠Crry同源。在用牛痘病毒感染后15至20小时，体外培养的KDH-8大鼠肝癌细胞显示出Crry样抗原表达的强烈降低，并且证明当将1：5稀释的正常大鼠血清作为补体来源添加到培养基中时，对补体沉积敏感。向用极低剂量的牛痘病毒（1空斑形成单位（PFU）/1000个细胞）感染的培养的KDH-8细胞中添加补体，显著降低了细胞培养物中病毒感染的扩散，而通过加热或zymozan处理灭活补体则消除了保护作用。
Decay accelerating factor (DAF), membrane cofactor protein (MCP), complement receptor 1 and mouse Crry are cell surface‐bound complement regulatory proteins capable of inhibiting C3 convertase activity on cell membranes, and therefore provide a substantial protection from attack by homologous complement activated either by the classical or by the alternative pathway. Decrease in complement regulatory activity might lead to spontaneous complement deposition and subsequent cell injury. MoAb 512 can inhibit the complement regulatory activity of molecules on rat cells, resulting in deposition of homologous complement. The antigen recognized by 512 MoAb in rats is homologous to mouse Crry. Fifteen to 20 h after infection with vaccinia virus, in vitro cultured KDH‐8 rat hepatoma cells show a strong decrease in expression of Crry‐like antigen, and proved to be sensitive to complement deposition when 1:5 diluted normal rat serum was added to the culture medium as a source of complement. Addition of complement to the cultured KDH‐8 cells infected with a very low dose of vaccinia virus (1 plaque‐forming unit (PFU)/1000 cells) substantially reduced spreading of virus infection in the cell culture, while inactivation of complement by heat or zymozan treatment abrogated the protective effect.
DOI：
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发表时间：
1989
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Paul,MS;Aegerter,M;O'Brien,SE;Kurtz,CB;Weis,JH
通讯作者：
Weis,JH
人 C5a 内负责刺激 IL-6 合成的效应器区域的鉴定和表征。
DOI：
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发表时间：
1992
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Morgan,EL;Sanderson,S;Scholz,W;Noonan,DJ;Weigle,WO;Hugli,TE
通讯作者：
Hugli,TE
人 IL-1 beta 转录与翻译的解离：在没有翻译的情况下通过粘附或重组 C5a 诱导稳态 mRNA。
DOI：
10.3181/00379727-200-43425
发表时间：
1992
期刊：
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
影响因子：
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作者：
Dinarello,CA
通讯作者：
Dinarello,CA