Ablation of @entity3414 (+) dendritic cell mediated cross-presentation does not impact atherosclerosis in hyperlipidemic XXXX .

@entity19 @entity3414 @entity41844
Clinical complications of atherosclerosis are almost exclusively linked to destabilization of the atherosclerotic plaque. @entity41844 -dependent dendritic cells specialize in cross-presentation of necrotic tissue-derived epitopes to directly activate cytolytic CD8 Tcells. The mature plaque (necrotic, containing dendritic cells and CD8 Tcells) could offer the ideal environment for cross-presentation, resulting in cytotoxic immunity and plaque destabilization. Ldlr(-/-) @entity19 were transplanted with @entity41844 (-/-) or wt bone marrow and put on a western type diet. Hematopoietic @entity41844 deficiency sharply decreased @entity3414 (+) DC numbers in spleen and lymph nodes (>80%; P   <   0,001). Concordantly, @entity41844 (-/-) chimeras had a 75% reduction in OT-I cross-priming capacity in vivo. @entity41844 (-/-) chimeric @entity19 did not show lower Tcell or other leukocyte subset numbers. Despite dampened cross-presentation capacity, @entity41844 (-/-) chimeras had equal atherosclerosis burden in aortic arch and root. Likewise, @entity41844 (-/-) chimeras and wt @entity19 revealed no differences in parameters of plaque stability: plaque Tcell infiltration, cell death, collagen composition, and macrophage and vascular smooth muscle cell content were unchanged. These results show that @entity3414 (+) DC loss in hyperlipidemic @entity19 profoundly reduces cross-priming ability, nevertheless it does not influence lesion development. Taken together, we clearly demonstrate that @entity3414 (+) DC-mediated cross-presentation does not significantly contribute to atherosclerotic plaque formation and stability.
