MHC Class II-Restricted Antigen Presentation by Plasmacytoid Dendritic Cells Drives Pro-Atherogenic T Cell Immunity Running title: Sage et al.; MHC II expression by pDC promotes atherosclerosis
نویسندگان
چکیده
Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom; Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom; Institut National de la Santé et de la Recherche Médicale, Unit 970, Paris Cardiovascular Research Center, Paris, France; Dept of Pharmacy, University of Naples Federico II, Naples, Italy; Institute of Immunobiology, Kantonal Hospital St. Gallen, St. Gallen, Switzerland; Dept of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Center for Molecular Medicine, Dept of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden; Dept of Microbiology and Immunology, Columbia University Medical Center, New York; Dept of Pathology, University of Geneva Medical School, Geneva, Switzerland
منابع مشابه
MHC Class II-restricted antigen presentation by plasmacytoid dendritic cells drives proatherogenic T cell immunity.
BACKGROUND Plasmacytoid dendritic cells (pDCs) bridge innate and adaptive immune responses and are important regulators of immuno-inflammatory diseases. However, their role in atherosclerosis remains elusive. METHODS AND RESULTS Here, we used genetic approaches to investigate the role of pDCs in atherosclerosis. Selective pDC deficiency in vivo was achieved using CD11c-Cre × Tcf4(-/flox) bone...
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RATIONALE Unlike conventional dendritic cells, plasmacytoid DCs (PDC) are poor in antigen presentation and critical for type I interferon response. Though proposed to be present in human atherosclerotic lesions, their role in atherosclerosis remains elusive. OBJECTIVE To investigate the role of PDC in atherosclerosis. METHODS AND RESULTS We show that PDC are scarcely present in human athero...
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تاریخ انتشار 2014