Lymphocytic tumor necrosis factor receptor superfamily co-stimulatory molecules in the pathogenesis of atherosclerosis
Lymphocytic tumor necrosis factor receptor superfamily co-stimulatory molecules in the pathogenesis of atherosclerosis
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DOI：
10.1097/mol.0000000000000025
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发表时间：
2013-12
影响因子：
4.4
通讯作者：
E. Smeets;Svenja Meiler;E. Lutgens
中科院分区：
文献类型：
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作者：
E. Smeets;Svenja Meiler;E. Lutgens
综述目的淋巴细胞在慢性炎症性疾病动脉粥样硬化中的作用在过去的十年中已经出现。异质性肿瘤坏死因子受体超家族的共刺激分子在淋巴细胞活化、增殖和分化中起关键作用。在这里，我们描述了四个肿瘤坏死因子受体超家族成员在动脉粥样硬化中的免疫调节特性和机制。最近的研究发现，CD 40/CD 40 L、OX 40 L/OX 40、CD 70/CD 27和CD 137/CD 137 L存在于人类动脉粥样硬化斑块中，并且在动脉粥样硬化中显示出强的免疫调节功能，导致在小鼠动脉粥样硬化模型中的致动脉粥样硬化或动脉粥样硬化保护作用。总结深入了解动脉粥样硬化中共刺激相互作用的免疫调节机制有助于临床利用这些相互作用治疗心血管疾病。
Purpose of review The role of lymphocytes in the chronic inflammatory disease atherosclerosis has emerged over the past decade. Co-stimulatory molecules of the heterogeneous tumor necrosis factor receptor superfamily play a pivotal role in lymphocyte activation, proliferation and differentiation. Here we describe the immune modulatory properties and mechanisms of four tumor necrosis factor receptor superfamily members in atherosclerosis. Recent findings CD40/CD40L, OX40L/OX40, CD70/CD27 and CD137/CD137L are present in human atherosclerotic plaques and have shown strong immune modulatory functions in atherosclerosis, resulting in either atherogenic or atheroprotective effects in mouse models of atherosclerosis. Summary Insight into the immune modulatory mechanisms of co-stimulatory interactions in atherosclerosis can contribute to clinical exploitation of these interactions in the treatment of cardiovascular disease.