Figure 6.

Dendritic cell (DC) maturation, proinflammatory cytokine production, and the subsequent T‐cell proliferation from plaque patients induced by oxidized low‐density lipoprotein (oxLDL) were suppressed by statins. DCs were generated from peripheral blood monocytes of patients who underwent carotid endarterectomy. The same protocol was used as that for DCs of normal donors. Briefly, DCs at day 6 were treated with 10 μg/mL oxLDL for 24 hours. An aliquot of DCs at day 5 were treated with 2 μmol/L atorvastatin for 24 hours, and continued with 2 μmol/L atorvastatin in the presence or absence of 10 μg/mL oxLDL for an additional 24 hours. A, The expression of CD80, CD86, CD83 and HLA‐DR was tested on day 7 DCs derived from patient blood. Figure depicts the expression of CD86 and CD83 tested by flow cytometry. A representative of 6 independent experiments is shown. B, Cytokine production in DC cultures derived from patient blood. Culture supernatants were collected after 24 hours treatment. Cytokine level was determined by ELISA. Results represent the mean±SD from 6 independent experiments. IL indicates interleukin; TGF, transforming growth factor; TNF, tumor necrosis factor. C, Percentage of CD4, CD8, CD45RO, CD45RA, CD25, and CD69/71 positive cells in plaque T cells are presented. Results represent the mean±SD generated from 5 plaques. Plaque mononuclear cells were isolated from single cell populations using the standard Ficoll‐Paque PLUS, and followed by T‐cell purification using Dynabeads^® Untouched^™ Human T Cells. D, Plaque T‐cell proliferation induced by oxLDL‐treated DC was suppressed by atorvastatin (AVA). After the indicated treatment for 24 hours, DCs derived from patient peripheral blood monocyte were washed and cocultured with autologous plaque T cells in triplicates for 5 days. Bromodeoxyuridine (BrdU) was present in the last 16 hours. **P<0.01, DC+oxLDL vs DC and DC+AVA+oxLDL. ^## P<0.01, DC+ (AVA)+oxLDL vs DC+oxLDL.