Immune and inflammatory mechanisms of atherosclerosis (*).
Immune and inflammatory mechanisms of atherosclerosis (*).
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DOI：
10.1146/annurev.immunol.021908.132620
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发表时间：
2009
影响因子：
29.7
通讯作者：
Ley K
中科院分区：
文献类型：
--
作者：
Galkina E;Ley K
动脉粥样硬化是一种由血液中低密度脂蛋白（LDL）胆固醇水平升高引起的大中型动脉壁炎症性疾病。虽然树突状细胞（DCs）和淋巴细胞存在于正常动脉的外膜中，但它们在人和小鼠动脉粥样硬化动脉中的数量大大增加，并且它们的分布发生变化。在动脉粥样硬化内膜病变中发现了巨噬细胞、DC、泡沫细胞、淋巴细胞和其他炎性细胞。在这些病变下，外膜白细胞聚集成簇，类似于三级淋巴组织。实验性干预可以减少可用的血液单核细胞的数量，巨噬细胞和大多数DC和泡沫细胞来源于单核细胞，并在不改变血脂的情况下减少动脉粥样硬化病变负荷。在致动脉粥样硬化的条件下，内皮细胞产生的一氧化氮减少，活性氧（ROS）和晚期糖基化终产物（AGE）的负担增加。使产生ROS的NADPH氧化酶或AGE受体失能具有有益效果。靶向炎性粘附分子也可减少动脉粥样硬化。相反，去除或阻断IL-10或TGF-β会加速动脉粥样硬化。调节性T细胞和分泌天然抗体的B1细胞具有动脉粥样硬化保护作用。本文综述了动脉粥样硬化的炎症和免疫机制。
Atherosclerosis is an inflammatory disease of the wall of large- and medium-sized arteries that is precipitated by elevated levels of low-density lipoprotein (LDL) cholesterol in the blood. Although dendritic cells (DCs) and lymphocytes are found in the adventitia of normal arteries, their number is greatly expanded and their distribution changed in human and mouse atherosclerotic arteries. Macrophages, DCs, foam cells, lymphocytes, and other inflammatory cells are found in the intimal atherosclerotic lesions. Beneath these lesions, adventitial leukocytes organize in clusters that resemble tertiary lymphoid tissues. Experimental interventions can reduce the number of available blood monocytes, from which macrophages and most DCs and foam cells are derived, and reduce atherosclerotic lesion burden without altering blood lipids. Under proatherogenic conditions, nitric oxide production from endothelial cells is reduced and the burden of reactive oxygen species (ROS) and advanced glycation end products (AGE) is increased. Incapacitating ROS-generating NADPH oxidase or the receptor for AGE (RAGE) has beneficial effects. Targeting inflammatory adhesion molecules also reduces atherosclerosis. Conversely, removing or blocking IL-10 or TGF-β accelerates atherosclerosis. Regulatory T cells and B1 cells secreting natural antibodies are atheroprotective. This review summarizes our current understanding of inflammatory and immune mechanisms in atherosclerosis.
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影响因子：
82.9
作者：
Ait-Oufella, H;Salomon, BL;Mallat, Z
通讯作者：
Mallat, Z
影响因子：
6
作者：
Bhatia, Vinay K.;Yun, Sheng;Haskard, Dorian O.
通讯作者：
Haskard, Dorian O.
影响因子：
15.9
作者：
Barry-Lane, PA;Patterson, C;Runge, MS
通讯作者：
Runge, MS
DOI：
10.1161/01.atv.0000173306.47722.ec
发表时间：
2005-08-01
影响因子：
8.7
作者：
Bodary, PF;Gu, SF;Eitzman, DT
通讯作者：
Eitzman, DT
影响因子：
37.8
作者：
Aslanian, Ara M.;Charo, Israel F.
通讯作者：
Charo, Israel F.