The potential role of IL-37 in atherosclerosis.

Bang-wei Wu, Q. Zeng, K. Meng, Qingwei Ji
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引用次数: 33

Abstract

Atherosclerosis is an inflammatory disease characterized by extensive lipid deposition and atherosclerotic plaque formation in the intima. Interleukin (IL)-37 is anti-inflammatory cytokine in the IL-1 ligand family. Given that IL-37 plays an important function in the development and progression of inflammatory and autoimmune diseases, it may be associated with the development of atherosclerosis. IL-37, which is normally expressed at low levels in peripheral blood mononuclear cells (PBMC), mainly monocytes, and dendritic cells (DC), is rapidly up-regulated in the inflammatory context, and therefore IL-37 conversely inhibits the production of inflammatory cytokines in PBMC and DC. In addition, IL-37 effectively suppresses the activation of macrophage and DC. It is not controversial that the activation of macrophage and DC and the over-expression of inflammatory cytokines are critical component elements in inflammatory process of atherosclerosis. Therefore, IL-37 may play a protective role in atherosclerosis through inhibition of inflammatory cytokines production and suppression of macrophage and DC activation.
IL-37在动脉粥样硬化中的潜在作用。
动脉粥样硬化是一种炎症性疾病,其特征是内膜内广泛的脂质沉积和动脉粥样硬化斑块的形成。白细胞介素(IL)-37是IL-1配体家族中的抗炎细胞因子。鉴于IL-37在炎症和自身免疫性疾病的发生发展中发挥重要作用,IL-37可能与动脉粥样硬化的发生发展有关。IL-37通常在外周血单核细胞(PBMC)(主要是单核细胞)和树突状细胞(DC)中低水平表达,在炎症环境下迅速上调,因此IL-37反过来抑制PBMC和DC中炎症细胞因子的产生。此外,IL-37还能有效抑制巨噬细胞和DC的活化。巨噬细胞和DC的激活以及炎症细胞因子的过度表达是动脉粥样硬化炎症过程的关键组成要素,这是没有争议的。因此,IL-37可能通过抑制炎症细胞因子的产生,抑制巨噬细胞和DC的激活,在动脉粥样硬化中发挥保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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