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白细胞介素-6在NZB/W F1小鼠免疫复合物介导的肾小球肾炎发病机制中的可能作用:诱导IgG类抗DNA自身抗体产生。

Possible role of IL-6 in pathogenesis of immune complex-mediated glomerulonephritis in NZB/W F1 mice: induction of IgG class anti-DNA autoantibody production.

作者信息

Mihara M, Ohsugi Y

机构信息

Fuji-Gotemba Research Laboratories, Chugai Pharmaceutical Co., Ltd., Shizuoka, Japan.

出版信息

Int Arch Allergy Appl Immunol. 1990;93(1):89-92. doi: 10.1159/000235285.

DOI:10.1159/000235285
PMID:2086490
Abstract

This study demonstrates that interleukin-6 (IL-6) increases the autoantibody production by B cells from NZB/W F1 mice. Splenic B cells were cultured for 5 days in the presence or absence of human IL-6, and then the anti-DNA antibody and immunoglobulin contents in the culture supernatants were measured by ELISA. Adding IL-6 increased IgG anti-DNA antibody production by B cells from old mice (30 weeks), but not from young ones (17 weeks). B cells obtained from both young and old mice produced IgM anti-DNA antibody, which increased when IL-6 was added. The increased anti-DNA antibody production was suppressed by anti-recombinant human IL-6 antibody to the background level, i.e. antibody contents in the absence of IL-6. In contrast, murine IL-5 did not increase IgG anti-DNA antibody production, although it promoted the production of IgM anti-DNA antibody. Furthermore, when IL-5 was added in combination with IL-6, there was an additive increase in IgM, but not in IgG anti-DNA antibody production. Similar results were obtained in the measurement of the immunoglobulin contents. These results suggest the possible role of IL-6 in the pathogenesis of autoimmune disease in NZB/W F1 mice.

摘要

本研究表明,白细胞介素-6(IL-6)可增加NZB/W F1小鼠B细胞的自身抗体产生。将脾B细胞在有或无人类IL-6的情况下培养5天,然后通过酶联免疫吸附测定法(ELISA)测量培养上清液中的抗DNA抗体和免疫球蛋白含量。添加IL-6可增加老年小鼠(30周龄)B细胞产生IgG抗DNA抗体,但对年轻小鼠(17周龄)的B细胞无此作用。从年轻和老年小鼠获得的B细胞均产生IgM抗DNA抗体,添加IL-6后其产量增加。抗重组人IL-6抗体可将增加的抗DNA抗体产生抑制至背景水平,即在无IL-6时的抗体含量水平。相比之下,鼠IL-5虽能促进IgM抗DNA抗体的产生,但不会增加IgG抗DNA抗体的产生。此外,当IL-5与IL-6联合添加时,IgM抗DNA抗体产量呈累加增加,但IgG抗DNA抗体产量无此变化。在免疫球蛋白含量测量中也得到了类似结果。这些结果提示IL-6在NZB/W F1小鼠自身免疫性疾病发病机制中可能发挥的作用。

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