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Activation of the alternative pathway of guinea pig complement by Sendai virus-treated cells.

作者信息

Okada N, Shibuta H, Okada H

出版信息

Microbiol Immunol. 1979;23(7):689-92. doi: 10.1111/j.1348-0421.1979.tb00511.x.

DOI:10.1111/j.1348-0421.1979.tb00511.x
PMID:228167
Abstract
摘要

相似文献

1
Activation of the alternative pathway of guinea pig complement by Sendai virus-treated cells.仙台病毒处理的细胞对豚鼠补体替代途径的激活。
Microbiol Immunol. 1979;23(7):689-92. doi: 10.1111/j.1348-0421.1979.tb00511.x.
2
Sendai virus infected cells are readily cytolysed by guinea-pig complement without antibody.仙台病毒感染的细胞很容易被豚鼠补体在无抗体的情况下溶解。
Immunology. 1981 Jun;43(2):337-44.
3
Cytolysis of Sendai virus-infected guinea-pig cells by homologous complement.同源补体对仙台病毒感染的豚鼠细胞的细胞溶解作用。
Immunology. 1983 May;49(1):29-35.
4
Activation of complement by antibodies to the keratosulphate-like host antigen of Sendai virus.通过针对仙台病毒硫酸角质素样宿主抗原的抗体激活补体。
Acta Pathol Microbiol Scand C. 1980 Apr;88(2):73-6. doi: 10.1111/j.1699-0463.1980.tb00075.x.
5
[Studies of the possible importance of complement in increasing the hemagglutination-inhibiting activity of rabbit IgM against Sendai virus].[关于补体在增强兔IgM对仙台病毒的血凝抑制活性中可能重要性的研究]
Boll Ist Sieroter Milan. 1978 Mar 31;57(1):54-9.
6
Neutralization of sendai virus by the IgG subclass antibodies of the guinea pig.
Microbiol Immunol. 1982;26(9):821-9. doi: 10.1111/j.1348-0421.1982.tb00228.x.
7
IgG and complement-mediated tissue damage in the absence of C2: evidence of a functionally active C2-bypass pathway in a guinea pig model.在缺乏C2的情况下IgG和补体介导的组织损伤:豚鼠模型中功能活跃的C2旁路途径的证据
J Immunol. 1999 Sep 15;163(6):3549-58.
8
Inhibition of the classical and alternative pathways of human and guinea pig complement by pyran copolymer.吡喃共聚物对人和豚鼠补体经典途径及替代途径的抑制作用
Int Arch Allergy Appl Immunol. 1981;66(3):304-9. doi: 10.1159/000232834.
9
Interaction of desialated guinea pig erythrocytes with the classical and alternative pathways of guinea pig complement in vivo and in vitro.去唾液酸豚鼠红细胞与豚鼠补体经典途径和替代途径在体内和体外的相互作用。
J Clin Invest. 1983 Jun;71(6):1710-9. doi: 10.1172/jci110925.
10
Prevention of complement activation on the homologous cell membrane of nucleated cells as well as erythrocytes.防止补体在有核细胞以及红细胞的同源细胞膜上激活。
Eur J Immunol. 1983 Apr;13(4):340-4. doi: 10.1002/eji.1830130413.

引用本文的文献

1
Complement Evasion Strategies of Viruses: An Overview.病毒的补体逃避策略:概述
Front Microbiol. 2017 Jun 16;8:1117. doi: 10.3389/fmicb.2017.01117. eCollection 2017.
2
Protective immune responses against West Nile virus are primed by distinct complement activation pathways.针对西尼罗河病毒的保护性免疫反应由不同的补体激活途径启动。
J Exp Med. 2006 May 15;203(5):1371-81. doi: 10.1084/jem.20052388. Epub 2006 May 1.
3
Appearance of complement components and immunoglobulins on nasopharyngeal epithelial cells following naturally acquired infection with respiratory syncytial virus.
呼吸道合胞病毒自然感染后鼻咽上皮细胞上补体成分和免疫球蛋白的出现情况。
J Med Virol. 1982;9(2):149-58. doi: 10.1002/jmv.1890090210.
4
Virus-induced complement activation and neutrophil-mediated cytotoxicity against respiratory syncytial virus (RSV).病毒诱导的补体激活以及中性粒细胞介导的针对呼吸道合胞病毒(RSV)的细胞毒性。
Clin Exp Immunol. 1984 Jun;56(3):501-8.
5
Cytolysis of Sendai virus-infected guinea-pig cells by homologous complement.同源补体对仙台病毒感染的豚鼠细胞的细胞溶解作用。
Immunology. 1983 May;49(1):29-35.
6
Sendai virus infected cells are readily cytolysed by guinea-pig complement without antibody.仙台病毒感染的细胞很容易被豚鼠补体在无抗体的情况下溶解。
Immunology. 1981 Jun;43(2):337-44.
7
Complement activation by respiratory syncytial virus-infected cells.呼吸道合胞病毒感染细胞引起的补体激活。
Arch Virol. 1986;88(1-2):49-56. doi: 10.1007/BF01310889.
8
Sensitization of human tumor cells to homologous complement by vaccinia virus treatment.通过牛痘病毒处理使人类肿瘤细胞对同源补体敏感。
Cancer Immunol Immunother. 1987;25(1):7-9. doi: 10.1007/BF00199294.
9
Effect of complement depletion by cobra venom factor on fowlpox virus infection in chickens and chicken embryos.眼镜蛇毒因子介导的补体耗竭对鸡和鸡胚中禽痘病毒感染的影响。
J Virol. 1986 Feb;57(2):670-3. doi: 10.1128/JVI.57.2.670-673.1986.
10
Tumor cells treated with vaccinia virus can activate the alternative pathway of mouse complement.用痘苗病毒处理的肿瘤细胞可激活小鼠补体的替代途径。
Jpn J Cancer Res. 1989 Aug;80(8):765-70. doi: 10.1111/j.1349-7006.1989.tb01712.x.