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系统性红斑狼疮中的细胞免疫

Cellular immunity in systemic lupus erythematosus.

作者信息

Boumpas D T, Eleftheriades E G, Tsokos G C

机构信息

Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

In Vivo. 1988 Jan-Feb;2(1):41-5.

PMID:2979815
Abstract

Production of pathogenic autoantibodies in patients with systemic lupus erythematosus (SLE) is the cornerstone in the pathogenesis of the disease. From the etiologic point of view, there is evidence that genetic, infectious, hormonal and environmental factors are essential to the development of SLE. The relative contribution of each group of factors to the expression of disease is individualized to each patient or group of patients with identical clinical disease. The cellular events which precede the B cell overactivity are crucial. T cells may produce excessive amounts of factors promoting B cell function, decreased amounts of suppressive factors or diminished cytotoxic ability to eliminate autoreactive T or B cells. The current understanding of lymphocyte and macrophage abnormalities are presented critically in this communication.

摘要

系统性红斑狼疮(SLE)患者体内致病性自身抗体的产生是该疾病发病机制的基石。从病因学角度来看,有证据表明遗传、感染、激素和环境因素对SLE的发生发展至关重要。每组因素对疾病表现的相对贡献因每个患者或具有相同临床疾病的患者群体而异。B细胞过度活跃之前的细胞事件至关重要。T细胞可能产生过量促进B细胞功能的因子,抑制性因子的量减少,或消除自身反应性T或B细胞的细胞毒性能力减弱。本文批判性地介绍了目前对淋巴细胞和巨噬细胞异常的认识。

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