CCL17-expressing dendritic cells are crucial for the development of atherosclerosis
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ABSTRACT: Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease.
ORGANISM(S): Mus musculus
PROVIDER: GSE13642 | GEO | 2011/11/01
SECONDARY ACCESSION(S): PRJNA110191
REPOSITORIES: GEO
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