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类风湿性关节炎淋巴细胞在体外对爱泼斯坦-巴尔病毒感染的异常反应:多种缺陷的证据

Abnormal responses of rheumatoid arthritis lymphocytes to Epstein-Barr virus infection in vitro: evidence for multiple defects.

作者信息

Irving W L, Walker P R, Lydyard P M

出版信息

Ann Rheum Dis. 1985 Jul;44(7):462-8. doi: 10.1136/ard.44.7.462.

DOI:10.1136/ard.44.7.462
PMID:2992398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1001677/
Abstract

Blood lymphocytes from 53 patients with rheumatoid arthritis (RA) and 44 controls were cultured with the polyclonal B cell activator Epstein-Barr virus (EBV). Culture supernatants were removed at weekly intervals and the amount of IgM secreted by the lymphocytes measured by an enzyme-linked immunosorbent assay (ELISA). Three major differences in the pattern of EBV-induced IgM synthesis by RA versus control lymphocytes were observed. Lymphocytes from RA patients, in general, produced less IgM after one week in culture than controls. In contrast, they increased their IgM secretion significantly by the end of the second week, whereas control lymphocyte cultures showed little change in IgM secretion at this time. Control lymphocytes from EBV seropositive individuals produced undetectable amounts of IgM after five weeks in culture. However, lymphocytes from 40% of the RA patients, even though they were EBV seropositive, secreted greater than 2000 ng/ml (microgram/l) IgM after five weeks. The data are discussed in terms of defective B and T cell responses to EBV in lymphocytes from patients with RA.

摘要

用多克隆B细胞激活剂爱泼斯坦-巴尔病毒(EBV)培养53例类风湿性关节炎(RA)患者和44例对照者的血液淋巴细胞。每周去除培养上清液,并用酶联免疫吸附测定(ELISA)法测定淋巴细胞分泌的IgM量。观察到RA患者与对照淋巴细胞在EBV诱导的IgM合成模式上有三个主要差异。一般来说,RA患者的淋巴细胞在培养一周后产生的IgM比对照者少。相反,到第二周结束时,它们的IgM分泌显著增加,而此时对照淋巴细胞培养物的IgM分泌几乎没有变化。来自EBV血清阳性个体的对照淋巴细胞在培养五周后产生的IgM量检测不到。然而,40%的RA患者的淋巴细胞,即使他们是EBV血清阳性,在五周后分泌的IgM大于2000 ng/ml(微克/升)。从RA患者淋巴细胞中B细胞和T细胞对EBV反应缺陷的角度对数据进行了讨论。

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本文引用的文献

1
Circulating activated lymphocytes in rheumatoid arthritis: a marker of synovial inflammation.类风湿关节炎中循环活化淋巴细胞:滑膜炎症的标志物。
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Interleukin-2 reverses deficient cell-mediated immune responses in rheumatoid arthritis.白细胞介素-2可逆转类风湿关节炎中细胞介导的免疫反应缺陷。
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Evidence for B cell activation in patients with active rheumatoid arthritis.活动性类风湿关节炎患者B细胞活化的证据。
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Epstein-Barr virus susceptibility of normal human B lymphocyte populations.正常人B淋巴细胞群体对爱泼斯坦-巴尔病毒的易感性。
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Effects of cyclosporin A on immunoglobulin production by EB virus stimulated lymphocytes.环孢菌素A对EB病毒刺激的淋巴细胞产生免疫球蛋白的影响。
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6
Frequencies of the separate human B cell subsets activatable to Ig secretion by Epstein-Barr virus and pokeweed mitogen.可被爱泼斯坦-巴尔病毒和商陆丝裂原激活分泌免疫球蛋白的不同人类B细胞亚群的频率。
J Exp Med. 1983 Jun 1;157(6):1808-14. doi: 10.1084/jem.157.6.1808.
7
Epstein-Barr virus-specific cytotoxic T cell responses in rheumatoid arthritis patients.类风湿关节炎患者中爱泼斯坦-巴尔病毒特异性细胞毒性T细胞反应
Rheumatol Int. 1982;2(4):155-9. doi: 10.1007/BF00286137.
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Analysis of the defects responsible for the impaired regulation of Epstein-Barr virus-induced B cell proliferation by rheumatoid arthritis lymphocytes. I. Diminished gamma interferon production in response to autologous stimulation.类风湿关节炎淋巴细胞导致爱泼斯坦-巴尔病毒诱导的B细胞增殖调节受损的缺陷分析。I. 自体刺激后γ干扰素产生减少。
J Exp Med. 1983 Jan 1;157(1):173-88. doi: 10.1084/jem.157.1.173.
9
Limiting dilution analysis of Epstein-Barr virus-induced immunoglobulin production by human B cells.爱泼斯坦-巴尔病毒诱导人B细胞产生免疫球蛋白的有限稀释分析。
J Exp Med. 1983 Jan 1;157(1):1-14. doi: 10.1084/jem.157.1.1.
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Impaired regulation of Epstein-Barr virus-induced lymphocyte proliferation in rheumatoid arthritis is due to a T cell defect.
J Immunol. 1981 Nov;127(5):1899-902.