Dendritic cells: An important link between antiphospholipid antibodies, endothelial dysfunction, and atherosclerosis in autoimmune and non-autoimmune diseases

被引:28
作者
Broder, Anna [1 ]
Chan, Jimmy J. [2 ]
Putterman, Chaim [1 ]
机构
[1] Montefiore Med Ctr, Albert Einstein Coll Med, Div Rheumatol, Bronx, NY 10461 USA
[2] Albert Einstein Coll Med, Bronx, NY 10461 USA
关键词
Dendritic cells; Antiphospholipid antibodies; Atherosclerosis; Antiphospholipid syndrome; LOW-DENSITY-LIPOPROTEIN; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CARDIOVASCULAR-DISEASES; BETA(2)-GLYCOPROTEIN I; BETA2-GLYCOPROTEIN I; IMMUNE-MECHANISMS; APOPTOTIC CELLS; KAPPA-B; BETA-2-GLYCOPROTEIN-I; AUTOANTIBODIES;
D O I
10.1016/j.clim.2012.12.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The presence of dendritic cells, antigen-presenting cells that link innate and adaptive immunity, is necessary to generate and maintain the production of antiphospholipid antibodies in response to exposed intracellular phospholipids on the outer surface of apoptotic cells. In turn, antiphospholipid antibodies enhance dendritic cell-induced inflammatory and proatherogenic responses in a number of conditions that are associated with accelerated atherosclerosis, including diabetes, chronic kidney disease, periodontal infections, and aging. While altering dendritic cells by modifying the ubiquitin proteasome system enhances antiphospholipid antibody production and leads to development of accelerated atherosclerosis and autoimmune features, inducing tolerance by dendritic cell manipulation leads to decreased atherosclerosis and thrombosis. Therefore, further translational studies are needed to understand the interplay between dendritic cells and antiphospholipid antibodies, and to develop potential new therapies for antiphospholipid syndrome and atherosclerosis. Here we review current experimental and translational studies that have examined the rote of dendritic cells in antiphospholipid antibody formation and in antiphospholipid-associated atherosclerosis and thrombosis. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:197 / 206
页数:10
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