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建立抗Yo抗体介导的副肿瘤性小脑变性动物模型的试验。2. 将用重组Yo蛋白激活的小鼠单核细胞被动转移至重度联合免疫缺陷小鼠的副肿瘤性小脑变性淋巴细胞中。

Trial to establish an animal model of paraneoplastic cerebellar degeneration with anti-Yo antibody. 2. Passive transfer of murine mononuclear cells activated with recombinant Yo protein to paraneoplastic cerebellar degeneration lymphocytes in severe combined immunodeficiency mice.

作者信息

Tanaka K, Tanaka M, Igarashi S, Onodera O, Miyatake T, Tsuji S

机构信息

Department of Neurology, Brain Research Institute, Niigata University, Japan.

出版信息

Clin Neurol Neurosurg. 1995 Feb;97(1):101-5. doi: 10.1016/0303-8467(95)00006-6.

Abstract

Passive transfer of serum IgG or mononuclear cells from peripheral blood of a patient with paraneoplastic cerebellar degeneration (PCD) to rodents was carried out in order to examine the role of anti-Purkinje cell antibody (anti-Yo antibody) present in serum and cerebrospinal fluid of PCD patients. After a single injection of IgG into mouse brain, it was taken up by Purkinje cells and remained there for more than 36 h without Purkinje cell loss. Injection of PCD IgG together with complement or lipopolysaccharide-activated human macrophages or rat mononuclear cells into rat ventricles did not cause Purkinje cell loss. We also studied passive transfer of the PCD patient's lymphocytes to mice with severe combined immunodeficiency (SCID). We constructed a recombinant Yo fusion protein that has the leucine-zipper protein (Yo protein), the common epitope for anti-Yo antibody for immunizing mice, and that resulted in production of significant amounts of anti-Yo antibody. Spleen cells from these Yo protein immunized mice were injected intravenously or intracerebrally into naive mice that subsequently showed no neurological symptoms or loss of Purkinje cells. We conclude that the anti-Yo antibody, either in combination with or without complement or activated mononuclear cells, cannot be the sole cause of Purkinje cell loss.

摘要

为了研究副肿瘤性小脑变性(PCD)患者血清和脑脊液中存在的抗浦肯野细胞抗体(抗Yo抗体)的作用,将PCD患者外周血中的血清IgG或单核细胞被动转移至啮齿动物体内。向小鼠脑内单次注射IgG后,它被浦肯野细胞摄取并在那里停留超过36小时,而没有浦肯野细胞丢失。将PCD IgG与补体或脂多糖激活的人巨噬细胞或大鼠单核细胞一起注射到大鼠脑室中不会导致浦肯野细胞丢失。我们还研究了将PCD患者的淋巴细胞被动转移至严重联合免疫缺陷(SCID)小鼠体内的情况。我们构建了一种重组Yo融合蛋白,其具有亮氨酸拉链蛋白(Yo蛋白),这是抗Yo抗体的共同表位,用于免疫小鼠,并导致产生大量抗Yo抗体。将来自这些经Yo蛋白免疫的小鼠的脾细胞静脉内或脑内注射到未出现神经症状或浦肯野细胞丢失的幼稚小鼠体内。我们得出结论,抗Yo抗体,无论是否与补体或活化的单核细胞结合,都不是浦肯野细胞丢失的唯一原因。

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