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系统性红斑狼疮、类风湿关节炎及其他风湿性疾病中的细胞因子谱。

Cytokine profile in systemic lupus erythematosus, rheumatoid arthritis, and other rheumatic diseases.

作者信息

al-Janadi M, al-Balla S, al-Dalaan A, Raziuddin S

机构信息

Department of Medicine, King Saud University, College of Medicine, Abha, Saudi Arabia.

出版信息

J Clin Immunol. 1993 Jan;13(1):58-67. doi: 10.1007/BF00920636.

DOI:10.1007/BF00920636
PMID:8445045
Abstract

We investigated serum levels of interleukin-6 (IL-6), interferon-gamma (IFN-gamma), and tumor necrosis factor alpha (TNF alpha) from patients with systemic lupus erythematosus (SLE) and its various clinical manifestations of disease and from patients with rheumatoid arthritis (RA) and other rheumatic diseases. The serum levels of IL-6 and IFN-gamma were highly elevated from patients with SLE associated with lymphadenopathy (LN) or nephrotic syndrome (NS). On the contrary, the serum levels of TNF alpha were elevated from most patients with SLE associated with thrombocytopenia (TP). However, serum levels of TNF alpha were in the normal range from patients with SLE associated with NS, LN, or central nervous system disease. Of interest, patients with SLE associated with humoral immunodeficiency disorder, hypogammaglobulinemia, had highly elevated levels of serum IL-6. The concanavalin A-stimulated mononuclear cells (MNC) of patients with SLE associated with TP secreted highly elevated levels of TNF alpha compared to other patient groups. We suggest that abnormal production of various cytokines in SLE is an intrinsic defect of MNC and the immune system that may be the key element for a variety of clinical manifestations of this disease.

摘要

我们研究了系统性红斑狼疮(SLE)患者及其各种疾病临床表现、类风湿关节炎(RA)患者和其他风湿性疾病患者的血清白细胞介素-6(IL-6)、干扰素-γ(IFN-γ)和肿瘤坏死因子α(TNFα)水平。与淋巴结病(LN)或肾病综合征(NS)相关的SLE患者的血清IL-6和IFN-γ水平显著升高。相反,大多数与血小板减少症(TP)相关的SLE患者的血清TNFα水平升高。然而,与NS、LN或中枢神经系统疾病相关的SLE患者的血清TNFα水平在正常范围内。有趣的是,与体液免疫缺陷疾病、低丙种球蛋白血症相关的SLE患者的血清IL-6水平显著升高。与其他患者组相比,与TP相关的SLE患者的伴刀豆球蛋白A刺激的单核细胞(MNC)分泌的TNFα水平显著升高。我们认为,SLE中各种细胞因子的异常产生是MNC和免疫系统的内在缺陷,这可能是该疾病各种临床表现的关键因素。

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本文引用的文献

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Mechanisms of Tumor Necrosis Factor-Alpha Inhibitor-Induced Systemic Lupus Erythematosus.肿瘤坏死因子-α抑制剂诱发系统性红斑狼疮的机制
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