Type I IFN signaling blockade by a PASylated antagonist during chronic SIV infection suppresses specific inflammatory pathways but does not alter T cell activation or virus replication.

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作者： Krystelle,Nganou-Makamdop ^[1] ; James M,Billingsley ^[2] ; Zachary,Yaffe ^[1] ; Gregory,O'Connor ^[1] ; Gregory K,Tharp ^[2] ; Amy,Ransier ^[1] ; Farida,Laboune ^[1] ; Rodrigo,Matus-Nicodemos ^[1] ; Andrea,Lerner ^[1] ; Lavina,Gharu ^[1] ; Jennifer M,Robertson ^[3] ; Mandy L,Ford ^[3] ; Martin,Schlapschy ^[4] ; Nadine,Kuhn ^[4] ; Alexandra,Lensch ^[4] ; Jeffrey,Lifson ^[5] ; Martha,Nason ^[6] ; Arne,Skerra ^[4] ; Gideon,Schreiber ^[7] ; Steven E,Bosinger ^[8] ; Daniel C,Douek ^[2]

作者单位： Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America. ^[1] Division of Microbiology and Immunology, Emory Vaccine Center, Yerkes National Primate Research Center, Atlanta, Georgia, United States of America. ^[2] Department of Surgery and Emory Transplant Center, Emory University School of Medicine and Emory Healthcare, Atlanta, GA. ^[3] Lehrstuhl für Biologische Chemie, Technische Universität München, Freising (Weihenstephan), Germany. ^[4] AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America. ^[5] Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America. ^[6] XL-protein GmbH, Freising, Germany. ^[7] Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel. ^[8] Department of Pathology & Laboratory Medicine, Emory University, Atlanta, Georgia, United States of America. ^[9]