TLR activation on CD11c+ DCs triggers DC maturation, which is critical for T cell activation. Given the expansion of CD11c+ DCs during the progression of atherosclerosis and the key role of T cell activation in atherogenesis, we sought to understand the role of TLR signaling in CD11c+ DCs in atherosclerosis. To this end, we used a mouse model in which a key TLR adaptor involved in DC maturation, MYD88, is deleted in CD11c+ DCs. We transplanted bone marrow containing
Manikandan Subramanian, Edward Thorp, Goran K. Hansson, Ira Tabas
Evidence that MyD88 deficiency in CD11c+ cells abrogates Treg-mediated suppression of MCP-1 and monocyte recruitment in the lesions of WD-fed