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人类动脉粥样硬化性腹主动脉瘤可产生白细胞介素(IL)-6和γ干扰素,但不产生IL-2和IL-4:IL-6和γ干扰素在血管炎症中的可能作用。

Human atherosclerotic abdominal aortic aneurysms produce interleukin (IL)-6 and interferon-gamma but not IL-2 and IL-4: the possible role for IL-6 and interferon-gamma in vascular inflammation.

作者信息

Szekanecz Z, Shah M R, Pearce W H, Koch A E

机构信息

Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.

出版信息

Agents Actions. 1994 Oct;42(3-4):159-62. doi: 10.1007/BF01983484.

DOI:10.1007/BF01983484
PMID:7879703
Abstract

Immunological mechanisms play an important role in the pathogenesis of atherosclerosis and atherosclerotic abdominal aortic aneurysms (AAA). Inflammatory leukocytes invade the vessel wall and produce cytokines which perpetuate the immune events underlying these diseases. Interleukin (IL)-1 beta, IL-8, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1, among others, may play a role in the generation by AAA. The aim of this study was to investigate the possible pathogenetic role of other proinflammatory cytokines, namely IL-2, IL-4, IL-6, and interferon (IFN)-gamma. Enzyme-linked immunosorbent assay of human explant culture supernatants revealed a significant increase in IFN-gamma production by AAA compared to occlusive (atherosclerotic) or normal (NL) aortic explants. IL-6 production was also increased in AAA compared to NL aortic explant supernatants. Neither AAA nor NL aortic tissues produced IL-2 or IL-4 in the same culture system. These results suggest that IL-6, a cytokine involved in T and B lymphocyte activation during inflammation, and IFN-gamma, which stimulates T and B lymphocytes, macrophages, endothelial cells and fibroblasts, may play a role in the pathogenesis of various vascular inflammatory diseases such as AAA.

摘要

免疫机制在动脉粥样硬化和动脉粥样硬化性腹主动脉瘤(AAA)的发病机制中起重要作用。炎性白细胞侵入血管壁并产生细胞因子,这些细胞因子使这些疾病潜在的免疫反应持续存在。白细胞介素(IL)-1β、IL-8、肿瘤坏死因子-α和单核细胞趋化蛋白-1等可能在AAA的发生中起作用。本研究的目的是调查其他促炎细胞因子,即IL-2、IL-4、IL-6和干扰素(IFN)-γ可能的致病作用。对人外植体培养上清液进行酶联免疫吸附测定显示,与闭塞性(动脉粥样硬化性)或正常(NL)主动脉外植体相比,AAA产生的IFN-γ显著增加。与NL主动脉外植体上清液相比,AAA中IL-6的产生也增加。在同一培养系统中,AAA和NL主动脉组织均未产生IL-2或IL-4。这些结果表明,IL-6是一种在炎症期间参与T和B淋巴细胞激活的细胞因子,而IFN-γ可刺激T和B淋巴细胞、巨噬细胞、内皮细胞和成纤维细胞,它们可能在诸如AAA等各种血管炎性疾病的发病机制中起作用。

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本文引用的文献

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Cytokines predict coronary aneurysm formation in Kawasaki disease patients.细胞因子可预测川崎病患者冠状动脉瘤的形成。
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Restricted cytokine expression in rheumatoid arthritis.类风湿关节炎中细胞因子表达受限
Signaling through the IL-6-STAT3 Pathway Promotes Proteolytically-Active Macrophage Accumulation Necessary for Development of Small AAA.
通过 IL-6-STAT3 通路的信号转导促进了蛋白水解活性的巨噬细胞的积累,这对于小 AAA 的发展是必要的。
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