我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

细胞因子在单核细胞致动脉硬化中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第2期
页码:
266-269，276
栏目:
综述
出版日期:
2010-12-10

文章信息/Info

Title:
-
作者:
陆文彬 综述; 沈成兴 审校
东南大学附属中大医院心内科，江苏 南京 210009
Author(s):
-
关键词:
单核细胞; 动脉粥样硬化; 细胞因子
Keywords:
-
分类号:
R543.5
DOI:
-
文献标识码:
A
摘要:
慢性炎症可导致动脉硬化，目前已经很清楚免疫细胞参与动脉硬化斑块的发病机制。白细胞的积聚和募集与动脉硬化斑块的形成有关，斑块的破裂可导致血栓、心梗或中风，最终导致死亡。斑块中绝大多数的巨噬细胞由单核细胞分化而来，单核细胞代表了循环系统中一类异质性的细胞群体。单核细胞在免疫系统的功能和炎症性疾病（如动脉硬化）中起着多重作用，而这些作用都涉及到细胞的运输和细胞迁移机制。本文回顾了近年来细胞因子在单核细胞迁移和渗出中作用的进展，着重介绍了主要的运输方式和调节单核细胞渗出的分子机制。
Abstract:
-

参考文献/References

[1]Auffray C, Sieweke MH, Geissmann F. Blood monocytes: development, heterogeneity, and relationship with dendritic cells［J］. Annu Rev Immunol, 2009, 27:669-692.

[2]Serbina NV, Pamer EG. Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2［J］. Nat Immunol, 2006, 7(3):311-317.

[3] Varol C, Landsman L, Fogg DK, et al. Monocytes give rise to mucosal,but not splenic, conventional dendritic cells［J］. J Exp Med, 2007, 204(1):171-180.

[4]Swirski FK, Nahrendorf M, Etzrodt M, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites［J］. Science, 2009, 325(5940):612-616.

[5] Nahrendorf M, Swirski FK, Aikawa E, et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions［J］. J Exp Med, 2007, 204(12):3037-3047.

[6]Huttenlocher A, Poznansky MC. Reverse leukocyte migration can be attractive or repulsive［J］. Trends Cell Biol, 2008, 18(6):298-306.

[7]Zernecke A, Shagdarsuren E, Weber C. Chemokines in atherosclerosis: an update［J］. Arterioscler Thromb Vasc Biol, 2008, 28(11):1897-1908.

[8]Phillipson M, Heit B, Colarusso P, et al. Intraluminal crawling of neutrophils to emigration sites: a molecularly distinct process from adhesion in the recruitment cascade［J］. J Exp Med, 2006, 203(12):2569-2575.

[9]Patel SS, Thiagarajan R, Willerson JT, et al. Inhibition of alpha4 integrin and ICAM-1 markedly attenuate macrophage homing to atherosclerotic plaques in ApoE-deficient mice［J］. Circulation, 1998, 97(1):75-81.

[10]Nakano H, Lin KL, Yanagita M, et al. Blood-derived inflammatory dendritic cells in lymph nodes stimulate acute T helper type 1 immune responses［J］. Nat Immunol, 2009, 10(4):394-402.

[11]Mishra RS, Carnevale KA, Cathcart MK. iPLA2beta: front and center in human monocyte chemotaxis to MCP-1［J］. J Exp Med, 2008, 205(2):347-359.

[12]Le Borgne M, Etchart N, Goubier A, et al. Dendritic cells rapidly recruited into epithelial tissues via CCR6/CCL20 are responsible for CD8+ T cell crosspriming in vivo［J］. Immunity, 2006, 24(2):191-201.

[13]Malik M, Chen YY, Kienzle MF, et al. Monocyte migration and LFA-1-mediated attachment to brain microvascular endothelia is regulated by SDF-1 alpha through Lyn kinase［J］. J Immunol, 2008, 181(7):4632-4637.

[14]ReShahrara S, Pickens SR, Dorfleutner A, et al. IL-17 induces monocyte migration in rheumatoid arthritis［J］. J Immunol, 2009, 182(6):3884-3891.

[15]Woollard KJ, Chin-Dusting J. Therapeutic targeting of p-selectin in atherosclerosis. Inflamm［J］. Allergy Drug Targets, 2007, 6(1):69-74.

[16]An G, Wang H, Tang R, et al. P-selectin glycoprotein ligand-1 is highly expressed on Ly-6Chi monocytes and a major determinant for Ly-6Chi monocyte recruitment to sites of atherosclerosis in mice［J］. Circulation, 2008, 117(25):3227-3237.

[17]Huo Y, Xia L. P-selectin glycoprotein ligand-1 plays a crucial role in the selective recruitment of leukocytes into the atherosclerotic arterial wall［J］. Trends Cardiovasc Med, 2009, 19(4):140-145.

[18]Woollard KJ, Suhartoyo A, Harris EE, et al. Pathophysiological levels of soluble P-selectin mediate adhesion of leukocytes to the endothelium through Mac-1 activation［J］. Circ Res, 2008, 103(10):1128-1138.

[19]Rohlena J, Volger OL, van Buul JD, et al. Endothelial CD81 is a marker of early human atherosclerotic plaques and facilitates monocyte adhesion［J］. Cardiovasc Res, 2009, 81(1):187-196.

[20]Auffray C, Fogg D, Garfa M, et al. Monitoring of blood vessels and tissues by a population of monocytes with patrolling behavior［J］. Science, 2007, 317(5838):666-670.

[21]Galkina E, Ley K. Vascular adhesion molecules in atherosclerosis［J］. Arterioscler Thromb Vasc Biol, 2007, 27(11):2292-2301.

[22]Choi EY, Chavakis E, Czabanka MA, et al. Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment［J］. Science, 2008, 322(5904):1101-1104.

[23]Liu DQ, Li LM, Guo YL, et al. Signal regulatory protein alpha negatively regula tes beta2 integrin-mediated monocyte adhesion, transendothelial migration and phagocytosis［J］. PLoS One, 2008, 3(9):e3291.

[24]Guo YL, Bai R, Chen CX, et al. Role of junctional adhesion molecule-like protein in mediating monocyte transendothelial migration［J］. Arterioscler Thromb Vasc Biol, 2009, 29(1):75-83.

[25]Korff T, Braun J, Pfaff D, et al. Role of ephrinB2 expression in endothelial cells during arteriogenesis: impact on smooth muscle cell migration and monocyte recruitment［J］. Blood, 2008, 112(1):73-81.

[26]Cayrol R, Wosik K, Berard JL, et al. Activated leukocyte cell adhesion molecule promotes leukocyte trafficking into the central nervous system［J］. Nat Immunol, 2008, 9(2):137-145.

[27]Bardin N, Blot-Chabaud M, Despoix N, et al. CD146 and its soluble form regulate monocyte transendothelial migration［J］. Arterioscler Thromb Vasc Biol, 2009, 29(5):746-753.

[28]Di Lorenzo A, Fernandez-Hernando C, Cirino G, et al. Akt1 is critical for acute inflammation and histamine-mediated vascular leakage［J］. Proc Natl Acad Sci U S A, 2009, 106(34):14552-14557.

[29]Zeng W, Li L, Yuan W, et al. A20 overexpression inhibits low shear flowinduced CD14-positive monocyte recruitment to endothelial cells［J］. Biorheology, 2009, 46(1):21-30.

[30]Hu Y, Hu X, Boumsell L, et al. IFN-gamma and STAT1 arrest monocyte migration and modulate RAC/CDC42 pathways［J］. J Immunol, 2008, 180(12):8057-8065.

[31]Hams E, Colmont CS, Dioszeghy V, et al. Oncostatin M receptor-beta signaling limits monocytic cell recruitment in acute inflammation［J］. J Immunol, 2008, 181(3):2174-2180.

[32]Seehaus S, Shahzad K, Kashif M, et al. Hypercoagulability inhibits monocyte transendothelial migration through protease-activated receptor-1-, phospholipase-C{beta}-, phosphoinositide 3-kinase-, and nitric oxide-dependent signaling in monocytes and promotes plaque stability［J］. Circulation, 2009, 120(9):774-784.

[33]朱毓,吴美华. 脂蛋白相关磷脂蛋白A2与动脉粥样硬化性疾病［J］. 心脏杂志, 2008, 20(1):101-103.

[34]傅羽,尹新华,张一娜. 组织因子途径抑制物与血管成形术后再狭窄［J］. 心脏杂志, 2008, 20(1):95-98.

[35]Patel SS, Thiagarajan R, Willerson JT, et al. Inhibition of alpha4 integrin and ICAM-1 markedly attenuate macrophage homing to atherosclerotic plaques in ApoE-deficient mice［J］. Circulation, 1998, 97(1):75-81.

备注/Memo

备注/Memo:
收稿日期：2010-03-25.通讯作者：沈成兴，副教授，博士，主要从事动脉粥样硬化机制研究 Email：shenchienx2@hotmail.com 作者简介：陆文彬，硕士生Email：luwenbingege@163.com
更新日期/Last Update: 2010-12-10