| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6087691 | Clinical Immunology | 2013 | 10 Pages |
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 role of dendritic cells in antiphospholipid antibody formation and in antiphospholipid-associated atherosclerosis and thrombosis.
⺠DCs link aPL Abs, APS, and atherosclerosis. ⺠DCs are needed to develop aPL Abs. ⺠aPL Abs promote DC maturation and pro-inflammatory functions. ⺠DC- aPL interactions are enhanced in conditions associated with atherosclerosis. ⺠DCs alterations may decrease DC-aPL interactions in APS and atherosclerosis.
