title: Ox-LDL can enhance the interaction of mice natural killer cells and dendritic cells via the CD48-2B4 pathway.
abstract: The importance of the interaction between natural killer (NK) cells and dendritic cells (DCs) in the expansion of antiviral and antitumor immune responses is well documented; however, limited information on NK/DC interaction during atherosclerosis is available. Inflammation plays an important role in the development of atherosclerosis, and oxidized low-density lipoprotein (ox-LDL) is believed to play a critical role in the development and progression of atherosclerosis. In this study, we developed a NK/DC coculture system to examine the role of ox-LDL in modulating the interaction of mice NK cells and DCs. Fresh NK cells were cocultured with DCs in the absence or presence of ox-LDL. We examined the cytokines released during the interaction. This report provides the first evidence of an enhancement effect by ox-LDL on the NK/DC crosstalk. Notably, we found that  ox-LDL significantly promoted the interaction of NK cells and DCs via CD48-2B4 contact-dependent mechanisms. These findings highlight the importance of NK/DCs crosstalk in atherosclerosis and provide new information about the possible mechanisms of atherosclerosis.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 79, Qingchun Road, Hangzhou, 310003, Zhejiang, China.
authors.forename: Kan
authors.initials: K
authors.lastname: Dong
authors.forename: Jun-Hua
authors.initials: JH
authors.lastname: Ge
authors.forename: Shu-Lian
authors.initials: SL
authors.lastname: Gu
authors.forename: Shan
authors.initials: S
authors.lastname: Li
authors.forename: Wei-Guo
authors.initials: WG
authors.lastname: Zhu
authors.forename: Fang-Yan
authors.initials: FY
authors.lastname: Fan
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Zhu
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism; D000071178:CD48 Antigen; D002450:Cell Communication; D018920:Coculture Techniques; D003602:Cytotoxicity, Immunologic; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D020014:K562 Cells; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D011971:Receptors, Immunologic / Q000378:metabolism*; D000071176:Signaling Lymphocytic Activation Molecule Family
chemical_list: D015703:Antigens, CD; D000071178:CD48 Antigen; C000604065:CD48 protein, human; C490007:Cd244a protein, mouse; C000604066:Cd48 protein, mouse; D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; D011971:Receptors, Immunologic; D000071176:Signaling Lymphocytic Activation Molecule Family; C099252:oxidized low density lipoprotein; D018664:Interleukin-12; D007371:Interferon-gamma