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乳酸脱氢酶升高病毒诱导的自身免疫:针对高尔基体抗原和其他亚细胞成分的单克隆自身抗体。

Autoimmunity induced by lactate dehydrogenase-elevating virus: monoclonal autoantibodies against Golgi antigens and other subcellular elements.

作者信息

Grossmann A, Weiland F, Weiland E

机构信息

Federal Research Centre for Virus Diseases of Animals, Tübingen, Federal Republic of Germany.

出版信息

Autoimmunity. 1989;2(3):201-11. doi: 10.3109/08916938909014684.

DOI:10.3109/08916938909014684
PMID:2491605
Abstract

Immunocompetent mice infected with LDVAGIA developed autoantibodies against Golgi antigen as early as 6-7 days postinfection preceding anti-viral antibodies for nearly a week. The anti-Golgi antibody titres peaked between two and three weeks postinfection independent of the applied virus dose. Already one week postinfection anti-Golgi autoantibodies were prominent in IgG subclasses IgG2a and b. Spleen cells from these mice were fused with myeloma cells and the culture fluids were screened by indirect immunofluorescence for antibodies reactive with the Golgi antigen of normal cultured cells. A panel of cloned stable antibody-producing hybridomas has been obtained. Some antibodies showed broad cross-species reactivity, recognizing similar antigenic determinants in the Golgi region of mouse, rat and other mammalian cells and also in avian and piscine cells, whereas others recognized determinants in this cell compartment only in mammalian cells and one recognized Golgi antigen only in particular murine tumor cells. From 19 Golgi antibody producing hybridomas 3 secreted IgM-antibodies, 10 synthesized autoantibodies of the subclass IgG2a and 6 of IgG2b. Applied in immunoelectron microscopy mABs decorated the Golgi organelle. A considerable amount of LDVAGIA-induced hybridomas produced antibodies against conserved antigens associated with the cytoskeleton, mitochondria, and the nucleus, LDV-induced monoclonal anti-Golgi antibodies decorated the Golgi area in LDV- and mock-infected macrophages. However, cytoplasmic fluorescence characteristic for LDV-infected cells was not observed indicating that the anti-Golgi autoantibodies do not cross-react with the virus.

摘要

感染LDVAGIA的免疫活性小鼠早在感染后6 - 7天就产生了针对高尔基体抗原的自身抗体,比抗病毒抗体早了近一周。抗高尔基体抗体滴度在感染后两到三周达到峰值,与所应用的病毒剂量无关。感染后仅一周,抗高尔基体自身抗体在IgG亚类IgG2a和b中就很显著。将这些小鼠的脾细胞与骨髓瘤细胞融合,通过间接免疫荧光筛选培养液中与正常培养细胞的高尔基体抗原反应的抗体。已获得一组克隆的稳定产生抗体的杂交瘤。一些抗体显示出广泛的跨物种反应性,能识别小鼠、大鼠和其他哺乳动物细胞以及禽类和鱼类细胞的高尔基体区域中相似的抗原决定簇,而其他抗体仅在哺乳动物细胞的这个细胞区室中识别决定簇,还有一种仅在特定的鼠类肿瘤细胞中识别高尔基体抗原。从19个产生高尔基体抗体的杂交瘤中,3个分泌IgM抗体,10个合成IgG2a亚类的自身抗体,6个合成IgG2b亚类的自身抗体。应用于免疫电子显微镜时,单克隆抗体可标记高尔基体细胞器。大量由LDVAGIA诱导产生的杂交瘤产生了针对与细胞骨架、线粒体和细胞核相关的保守抗原的抗体,LDV诱导的单克隆抗高尔基体抗体可标记LDV感染和模拟感染的巨噬细胞中的高尔基体区域。然而,未观察到LDV感染细胞特有的细胞质荧光,这表明抗高尔基体自身抗体不与病毒发生交叉反应。

相似文献

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Autoimmunity induced by lactate dehydrogenase-elevating virus: monoclonal autoantibodies against Golgi antigens and other subcellular elements.乳酸脱氢酶升高病毒诱导的自身免疫:针对高尔基体抗原和其他亚细胞成分的单克隆自身抗体。
Autoimmunity. 1989;2(3):201-11. doi: 10.3109/08916938909014684.
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Immunization with inactivated lactate dehydrogenase-elevating virus followed by virus infection favors the selection of hybridomas synthesizing antibodies cross-reacting with intermediate filaments and the LDV envelope protein VP3.
Autoimmunity. 1991;8(4):329-33. doi: 10.3109/08916939109007641.
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Lactate dehydrogenase-elevating virus induces anti-Golgi apparatus antibodies.乳酸脱氢酶升高病毒诱导抗高尔基体抗体。
J Gen Virol. 1987 Jul;68 ( Pt 7):1983-91. doi: 10.1099/0022-1317-68-7-1983.
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Characteristics of monoclonal antibodies to the lactate dehydrogenase-elevating virus.抗乳酸脱氢酶升高病毒单克隆抗体的特性
Intervirology. 1987;27(1):53-60. doi: 10.1159/000149715.
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Differential anti-Golgi complex autoantibody production following murine lactate dehydrogenase-elevating virus infection.小鼠乳酸脱氢酶升高病毒感染后抗高尔基体复合体自身抗体的差异产生
Immunopharmacol Immunotoxicol. 2008;30(1):13-25. doi: 10.1080/08923970701812191.
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Autoantibodies against golgi apparatus induced by arteriviruses.动脉病毒诱导产生的针对高尔基体的自身抗体。
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Monoclonal anti-IgG autoantibodies derived from lipopolysaccharide-activated spleen cells of 129/Sv mice.源自129/Sv小鼠脂多糖激活脾细胞的单克隆抗IgG自身抗体。
J Exp Med. 1982 Jan 1;155(1):219-30. doi: 10.1084/jem.155.1.219.
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Polyclonal B cell activation of IgG2a and IgG2b production by infection of mice with lactate dehydrogenase-elevating virus is partly dependent on CD4+ lymphocytes.通过用乳酸脱氢酶升高病毒感染小鼠来激活产生IgG2a和IgG2b的多克隆B细胞,部分依赖于CD4 +淋巴细胞。
Viral Immunol. 1990 Winter;3(4):273-88. doi: 10.1089/vim.1990.3.273.
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Virus-induced autoimmunity: monoclonal antibodies that react with endocrine tissues.病毒诱导的自身免疫:与内分泌组织发生反应的单克隆抗体。
Science. 1983 Apr 15;220(4594):304-6. doi: 10.1126/science.6301002.
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Neonatal infection of mice with lactate dehydrogenase-elevating virus results in suppression of humoral antiviral immune response but does not alter the course of viraemia or the polyclonal activation of B cells and immune complex formation.新生小鼠感染乳酸脱氢酶升高病毒会导致体液抗病毒免疫反应受到抑制,但不会改变病毒血症的进程,也不会改变B细胞的多克隆激活及免疫复合物的形成。
J Gen Virol. 1994 May;75 ( Pt 5):1071-81. doi: 10.1099/0022-1317-75-5-1071.

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