作者: Jing Wang , Chongxiu Sun , Norbert Gerdes , Conglin Liu , Mengyang Liao
DOI: 10.1038/NM.3890
关键词:
摘要: Abstract Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms,. Interruption of IL18 action reduces atherosclerosis in mice,. Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells. As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12 …