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类风湿关节炎患者外周血B细胞在体外产生白细胞介素1的能力增强。

Increased ability of peripheral blood B cells from patients with rheumatoid arthritis to produce interleukin 1 in vitro.

作者信息

Yamamura M, Nishiya K, Ota Z

机构信息

Third Department of Internal Medicine, Okayama University Medical School, Japan.

出版信息

Acta Med Okayama. 1990 Dec;44(6):301-8. doi: 10.18926/AMO/30433.

Abstract

Twenty-four patients with rheumatoid arthritis (RA) and 20 normal controls were examined for the ability of their peripheral blood B cells to produce interleukin 1 (IL-1) with or without lipopolysaccharide (LPS). B cells were purified from peripheral blood by negative selection methods (i.e., removal of adherent cells and sheep red blood cell rosette-forming cells, followed by treatment with monoclonal antibodies (OKT3 and OKM1) and complement). The amount of IL-1 in B cell culture supernatants (SN) was measured by thymocyte and fibroblast proliferation assays and an enzyme-linked immunosorbent assay for IL-1 alpha and beta. As a group, cultured B cells from patients with RA, both spontaneously and when stimulated with LPS, produced higher levels of IL-1 than those from normal controls. IL-1 production by RA B cells with LPS had a weak but positive correlation with disease activity. Moreover, RA B cell culture SN with elevated levels of IL-1 had a synergistic effect on the growth of anti-human IgM (anti-mu) stimulated B cells. In separate experiments, the growth of RA B cells was significantly promoted by IL-1 beta both with and without anti-mu stimulation. These results suggest that B cell-derived IL-1 may be involved in the B cell clonal expansion of RA through its own activity as a B cell stimulatory factor.

摘要

对24例类风湿性关节炎(RA)患者和20名正常对照者进行检测,观察其外周血B细胞在有或无脂多糖(LPS)刺激下产生白细胞介素1(IL-1)的能力。通过阴性选择方法(即去除贴壁细胞和形成绵羊红细胞花环的细胞,随后用单克隆抗体(OKT3和OKM1)及补体处理)从外周血中纯化B细胞。采用胸腺细胞和成纤维细胞增殖试验以及针对IL-1α和β的酶联免疫吸附试验来测定B细胞培养上清液(SN)中IL-1的含量。总体而言,RA患者的培养B细胞无论是自发产生还是在LPS刺激下产生的IL-1水平均高于正常对照者。RA B细胞在LPS刺激下产生IL-1的水平与疾病活动度呈弱但正相关。此外,IL-1水平升高的RA B细胞培养SN对抗人IgM(抗μ)刺激的B细胞生长具有协同作用。在单独的实验中,无论有无抗μ刺激,IL-1β均能显著促进RA B细胞的生长。这些结果提示,B细胞源性IL-1可能通过其作为B细胞刺激因子的自身活性参与RA的B细胞克隆性扩增。

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