Emergence of dendritic cells in rupture-prone regions of vulnerable carotid plaques

被引:265
作者
Yilmaz, A
Lochno, M
Traeg, F
Cicha, I
Reiss, C
Stumpf, C
Raaz, D
Anger, T
Amann, K
Probst, T
Ludwig, J
Daniel, WG
Garlichs, CD
机构
[1] Univ Erlangen Nurnberg, Med Clin 2, D-91054 Erlangen, Germany
[2] Univ Erlangen Nurnberg, Dept Pathol, D-91052 Erlangen, Germany
[3] Clin Nuremberg, Dept Vasc Surg, D-90340 Nurnberg, Germany
关键词
atherosclerosis; carotid stenosis; inflammation; plaque destabilization; antigen presentation; dendritic cells;
D O I
10.1016/j.atherosclerosis.2004.04.027
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Dendritic cells (DC), which are critically involved in various immunological disorders, were detected in atherosclerotic plaques in 1995. Since DC might be related to the immunological processes in atherosclerosis (AS), we analyzed the emergence of DC and other inflammatory cells in different stages of AS. Serial cross-sections of 44 carotid specimens were immunohistochemically analyzed for the presence of DC, T cells, macrophages, and HLA-DR. Atherosclerotic specimens were histologically defined as initial lesions, advanced stable, or vulnerable plaques. In initial lesions significantly lower DC numbers were detected than in advanced plaques (P < 0.001). For advanced plaques, DC numbers were significantly higher in vulnerable than in stable plaques (P = 0.005). In contrast to initial lesions, approximately 70% of DC in advanced plaques exhibited a mature phenotype (CD83(+), DC-LAMP(+)), indicating a functional activity of DC. In plaques of patients with acute ischemic symptoms DC numbers were markedly elevated (P = 0.03), whereas significantly lower DC numbers and more often a stable plaque morphology were detected in statin-treated patients (P = 0.02). DC clusters with a strong HLA-DR expression and frequent DC-T cell contacts were located particularly in the rupture-prone plaque regions and at complications. The results of the present study indicate that DC might contribute to plaque destabilization through an activation of T cells. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:101 / 110
页数:10
相关论文
共 31 条
[21]  
Mosialos G, 1996, AM J PATHOL, V148, P593
[22]   From vulnerable plaque to vulnerable patient - A call for new definitions and risk assessment strategies: Part I [J].
Naghavi, M ;
Libby, P ;
Falk, E ;
Casscells, SW ;
Litovsky, S ;
Rumberger, J ;
Badimon, JJ ;
Stefanadis, C ;
Moreno, P ;
Pasterkamp, G ;
Fayad, Z ;
Stone, PH ;
Waxman, S ;
Raggi, P ;
Madjid, M ;
Zarrabi, A ;
Burke, A ;
Yuan, C ;
Fitzgerald, PJ ;
Siscovick, DS ;
de Korte, CL ;
Aikawa, M ;
Airaksinen, KEJ ;
Assmann, G ;
Becker, CR ;
Chesebro, JH ;
Farb, A ;
Galis, ZS ;
Jackson, C ;
Jang, IK ;
Koenig, W ;
Lodder, RA ;
March, K ;
Demirovic, J ;
Navab, M ;
Priori, SG ;
Rekhter, MD ;
Bahr, R ;
Grundy, SM ;
Mehran, R ;
Colombo, A ;
Boerwinkle, E ;
Ballantyne, C ;
Insull, W ;
Schwartz, RS ;
Vogel, R ;
Serruys, PW ;
Hansson, GK ;
Faxon, DP ;
Kaul, S .
CIRCULATION, 2003, 108 (14) :1664-1672
[23]   Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries [J].
Pasterkamp, G ;
Schoneveld, AH ;
van der Wal, AC ;
Hijnen, DJ ;
van Wolveren, WJA ;
Plomp, S ;
Teepen, HLJM ;
Borst, C .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (01) :54-58
[24]   Atherosclerosis is an inflammatory disease [J].
Ross, R .
AMERICAN HEART JOURNAL, 1999, 138 (05) :S419-S420
[25]   AUTOANTIBODY AGAINST OXIDIZED LDL AND PROGRESSION OF CAROTID ATHEROSCLEROSIS [J].
SALONEN, JT ;
YLAHERTTUALA, S ;
YAMAMOTO, R ;
BUTLER, S ;
KORPELA, H ;
SALONEN, R ;
NYYSSONEN, K ;
PALINSKI, W ;
WITZTUM, JL .
LANCET, 1992, 339 (8798) :883-887
[26]   T-LYMPHOCYTES FROM HUMAN ATHEROSCLEROTIC PLAQUES RECOGNIZE OXIDIZED LOW-DENSITY-LIPOPROTEIN [J].
STEMME, S ;
FABER, B ;
HOLM, J ;
WIKLUND, O ;
WITZTUM, JL ;
HANSSON, GK .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (09) :3893-3897
[27]   Atherosclerotic plaque rupture - pathologic basis of plaque stability and instability [J].
van der Wal, AC ;
Becker, AE .
CARDIOVASCULAR RESEARCH, 1999, 41 (02) :334-344
[28]   SITE OF INTIMAL RUPTURE OR EROSION OF THROMBOSED CORONARY ATHEROSCLEROTIC PLAQUES IS CHARACTERIZED BY AN INFLAMMATORY PROCESS IRRESPECTIVE OF THE DOMINANT PLAQUE MORPHOLOGY [J].
VANDERWAL, AC ;
BECKER, AE ;
VANDERLOOS, CM ;
DAS, PK .
CIRCULATION, 1994, 89 (01) :36-44
[29]   Lessons from sudden coronary death - A comprehensive morphological classification scheme for atherosclerotic lesions [J].
Virmani, R ;
Kolodgie, FD ;
Burke, AP ;
Farb, A ;
Schwartz, SM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (05) :1262-1275
[30]   Endothelial determinants of dendritic cell adhesion and migration - New implications for vascular diseases [J].
Weis, M ;
Schlichting, CL ;
Engleman, EG ;
Cooke, JP .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (11) :1817-1823