The Regulation and Consequences of Immune-Mediated Cell Death in Atheromatous Diseases

被引:10
作者
Jonathan C. Choy
Thomas J. Podor
Bobby Yanagawa
John C. K. Lai
David J. Granville
David C. Walker
Bruce M. McManus
机构
[1] Dept. of Pathol. and Lab. Medicine, St. Paul's Hosp./Provid. Hlth. Care, University of British Columbia, Vancouver, BC
[2] McDonald Research Laboratories, iCAPTUR4E Centre, St. Paul's Hospital, Vancouver
基金
加拿大健康研究院;
关键词
Apoptosis; Coronary artery disease; FasL; Granzyme B; T-cell; Transplant vascular disease;
D O I
10.1385/CT:3:3:269
中图分类号
学科分类号
摘要
Atheromatous diseases are lipid and cell-rich vascular disorders that include coronary artery disease (CAD), transplant vascular disease (TVD), and restenosis. Considering the inflammatory nature of these diseases, cytotoxic immune mechanisms such as the FasL and granzyme/perforin pathways most likely play important roles in the development and remodeling of many lesions. Furthermore, although the contributions of immune responses to each disease vary, the correspondent localization of certain mediators and effectors suggests that they may contribute to a spectrum of atheromatous diseases. In this review, the contribution of immune cell-mediated cell death in the onset and pathogenesis of CAD and TVD is examined.
引用
收藏
页码:269 / 282
页数:13
相关论文
共 95 条
[51]  
Shi C., Lee W.S., He Q., Zhang D., Fletcher D.L. Jr., Newell J.B., Haber E., Immunologic basis of transplant-associated arteriosclerosis, Proc. Natl. Acad. Sci. USA, 93, pp. 4051-4056, (1996)
[52]  
Szeto W.Y., Krasinskas A.M., Kreisel D., Krupnick A.S., Popma S.H., Rosengard B.R., Depletion of recipient CD4+ but not CD8+ T lymphocytes prevents the development of cardiac allograft vasculopathy, Transplantation, 73, pp. 1116-1122, (2002)
[53]  
Fischbein M.P., Yun J., Laks H., Irie Y., Fishbein M.C., Espejo M., Bonavida B., Ardehali A., CD8+ lymphocytes augment chronic rejection in a MHC class II mismatched model, Transplantation, 71, pp. 1146-1153, (2001)
[54]  
Boyle J.J., Association of coronary plaque rupture and atherosclerotic inflammation, J. Pathol., 181, pp. 93-99, (1997)
[55]  
Jacob T., Ascher E., Hingorani A., Khandros Y., Tsemekhin B., Zeien L., Et al., Differential proteolytic activity and induction of apoptosis in fibrous versus atheromatous plaques in carotid atherosclerotic disease, J. Vasc. Surg., 33, pp. 614-620, (2001)
[56]  
Dong C., Wilson J.E., Winters G.L., McManus B.M., Human transplant coronary artery disease: Pathological evidence for Fas- mediated apoptotic cytotoxicity in allograft arteriopathy, Lab. Invest., 74, pp. 921-931, (1996)
[57]  
Subbotin V., Sun H., Aitouche A., Salam A., Valdivia L.A., Fung J.J., Et al., Marked mitigation of transplant vascular sclerosis in FasLg1d (CD95L) mutant recipients. The role of alloantibodies in the development of chronic rejection, Transplantation, 67, pp. 1295-1300, (1999)
[58]  
Wang T., Dong C., Stevenson S.C., Herderick E.E., Marshall-Neff J., Vasudevan S.S., Et al., Over-expression of soluble fas attenuates transplant arteriosclerosis in rat aortic allografts, Circulation, 106, pp. 1536-1542, (2002)
[59]  
Schiller N.K., Boisvert W.A., Curtiss L.K., Inflammation in atherosclerosis: Lesion formation in LDL receptor-deficient mice with perforin and Lyst(beige) mutations, Arterioscler. Thromb. Vasc. Biol., 22, pp. 1341-1346, (2002)
[60]  
Nakajima T., Schulte S., Warrington K.J., Kopecky S.L., Frye R.L., Goronzy J.J., Et al., T-cell-mediated lysis of endothelial cells in acute coronary syndromes, Circulation, 105, pp. 570-575, (2002)