Browsing by Author "Riken Research Center for Allergy and Immunology"

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    Glycan engineering of the sars-cov-2 receptor-binding domain elicits cross-neutralizing antibodies for sars-related viruses
    (2021-12-06) Ryo Shinnakasu; Shuhei Sakakibara; Hiromi Yamamoto; Po Hung Wang; Saya Moriyama; Nicolas Sax; Chikako Ono; Atsushi Yamanaka; Yu Adachi; Taishi Onodera; Takashi Sato; Masaharu Shinkai; Ryosuke Suzuki; Yoshiharu Matsuura; Noritaka Hashii; Yoshimasa Takahashi; Takeshi Inoue; Kazuo Yamashita; Tomohiro Kurosaki; Faculty of Tropical Medicine, Mahidol University; WPI Immunology Frontier Research Center, Osaka University; National Institute of Infectious Diseases; Research Institute for Microbial Diseases; Riken Research Center for Allergy and Immunology; Osaka University; National Institute of Health Sciences Tokyo; Tokyo Shinagawa Hospital; National Institute of Infection Diseases
    Broadly protective vaccines against SARS-related coronaviruses that may cause future outbreaks are urgently needed. The SARS-CoV-2 spike receptor-binding domain (RBD) comprises two regions, the core-RBD and the receptor-binding motif (RBM); the former is structurally conserved between SARS-CoV-2 and SARS-CoV. Here, in order to elicit humoral responses to the more conserved core-RBD, we introduced N-linked glycans onto RBM surfaces of the SARS-CoV-2 RBD and used them as immunogens in a mouse model. We found that glycan addition elicited higher proportions of the core-RBD–specific germinal center (GC) B cells and antibody responses, thereby manifesting significant neutralizing activity for SARS-CoV, SARS-CoV-2, and the bat WIV1-CoV. These results have implications for the design of SARS-like virus vaccines.
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    Human Proteinpedia enables sharing of human protein data [4]
    (2008-02-01) Suresh Mathivanan; Mukhtar Ahmed; Natalie G. Ahn; Hainard Alexandre; Ramars Amanchy; Philip C. Andrews; Joel S. Bader; Brian M. Balgley; Marcus Bantscheff; Keiryn L. Bennett; Erik Björling; Blagoy Blagoev; Ron Bose; Samir K. Brahmachari; Alma S. Burlingame; Xosé R. Bustelo; Gerard Cagney; Greg T. Cantin; Helene L. Cardasis; Julio E. Celis; Raghothama Chaerkady; Feixia Chu; Philip A. Cole; Catherine E. Costello; Robert J. Cotter; David Crockett; James P. DeLany; Angelo M. De Marzo; Leroi V. DeSouza; Eric W. Deutsch; Eric Dransfield; Gerard Drewes; Arnaud Droit; Michael J. Dunn; Kojo Elenitoba-Johnson; Rob M. Ewing; Jennifer Van Eyk; Vitor Faca; Jayson Falkner; Xiangming Fang; Catherine Fenselau; Daniel Figeys; Pierre Gagné; Cecilia Gelfi; Kris Gevaert; Jeffrey M. Gimble; Florian Gnad; Renu Goel; Pavel Gromov; Samir M. Hanash; William S. Hancock; H. C. Harsha; Gerald Hart; Faith Hays; Fuchu He; Prashantha Hebbar; Kenny Helsens; Heiko Hermeking; Winston Hide; Karin Hjernø; Denis F. Hochstrasser; Oliver Hofmann; David M. Horn; Ralph H. Hruban; Nieves Ibarrola; Peter James; Ole N. Jensen; Pia Hønnerup Jensen; Peter Jung; Kumaran Kandasamy; Indu Kheterpal; Reiko F. Kikuno; Ulrike Korf; Roman Körner; Bernhard Kuster; Min Seok Kwon; Hyoung Joo Lee; Young Jin Lee; Michael Lefevre; Minna Lehvaslaiho; Pierre Lescuyer; Fredrik Levander; Megan S. Lim; Christian Löbke; Institute of Bioinformatics; Johns Hopkins University; The Johns Hopkins School of Medicine; Kuvempu University; University of Colorado at Boulder; Universite de Geneve Faculte de Medecine; Calibrant Biosystems, Inc.; Cellzome AG; Osterreichische Akademie Der Wissenschaften; AlbaNova University Center; Syddansk Universitet; Institute of Genomics and Integrative Biology India; University of California, San Francisco; CSIC-USAL - Instituto de Biologia Molecular y Celular del Cancer de Salamanca (IBMCC); University College Dublin; Scripps Research Institute; NYU School of Medicine; Dansk Center For Translationel Brystkraeftforskning; Boston University School of Medicine; University of Michigan Medical School; University of Pittsburgh; York University; Institute for Systems Biology; TI Food and Nutrition; Universite Laval; Transition Therapeutics; Infochromics; Johns Hopkins Bayview Medical Center; Fred Hutchinson Cancer Research Center; GenWay Biotech Inc.; University of Maryland; University of Ottawa, Canada; Universita degli Studi di Milano; Department of Biochemistry and Medical Protein Research; Pennington Biomedical Research Center; Max Planck Institute of Biochemistry; Northeastern University; Beijing Institute of Radiation Medicine; Fudan University Shanghai Medical College; University of the Western Cape; Hopitaux universitaires de Geneve; Agilent Technologies; Johns Hopkins Medical Institutions; Lunds Universitet; Kazusa DNA Research Institute; German Cancer Research Center; Yonsei University; University of California, Davis; University of California, Los Angeles; European Bioinformatics Institute; Universitat de Barcelona; University of Michigan, Ann Arbor; Hanover; Hospital for Sick Children University of Toronto; University of Toronto; Ludwig Institute for Cancer Research Melbourne; INRA Centre de Clermont-Ferrand-Theix; North Carolina State University; Riken Research Center for Allergy and Immunology; Institute of Medical Science The University of Tokyo; European Molecular Biology Laboratory Heidelberg; George Mason University; Pacific Northwest National Laboratory; Helsingin Yliopisto; University of Tampere Institute of Medical Technology; David Geffen School of Medicine at UCLA; Centre for Cellular and Molecular Biology india; Mahidol University; SAIC-Frederick; Imperial College London
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    Prostaglandin E2-prostoglandin E receptor subtype 4 (EP4) signaling mediates UV irradiation-induced systemic immunosuppression
    (2011-04-19) Kitipong Soontrapa; Tetsuya Honda; Daiji Sakata; Chengcan Yao; Takako Hirata; Shohei Hori; Toshiyuki Matsuoka; Yoshihiro Kita; Takao Shimizu; Kenji Kabashima; Shuh Narumiya; Kyoto University Faculty of Medicine; Mahidol University; Riken Research Center for Allergy and Immunology; Graduate School of Medicine and Faculty of Medicine, The University of Tokyo
    UV radiation induces systemic immunosuppression. Because nonsteroidal anti-inflammatory drugs suppress UV-induced immunosuppression, prostanoids have been suspected as a crucial mediator of this UV effect. However, the identity of the prostanoid involved and its mechanism of action remain unclear. Here, we addressed this issue by subjecting mice deficient in each prostanoid receptor individually or mice treated with a subtype-specific antagonist to UV irradiation. Mice treated with an antagonist for prostaglandin E receptor subtype 4 (EP4), but not those deficient in other prostanoid receptors, show impaired UV-induced immunosuppression, whereas administration of an EP4 agonist rescues the impairment of the UV-induced immunosuppression in indomethacin-treated mice. The EP4 antagonist treatment suppresses an increase in the number of CD4 + /forkhead box P3-positive (Foxp3 + ) regulatory T cells (Treg cells) in the peripheral lymph nodes (LNs) and dendritic cells expressing DEC205 in the LNs and the skin after UV irradiation. Furthermore, the EP4 antagonist treatment down-regulates UV-induced expression of receptor activator of NF-κB ligand (RANKL) in skin keratinocytes. Finally, administration of anti-RANKL antibody abolishes the restoration of UV-induced immunosuppression by EP4 agonism in indomethacin-treated mice. Thus, prostaglandin E 2 (PGE 2 )-EP4 signaling mediates UV-induced immunosuppression by elevating the number of Treg cells through regulation of RANKL expression in the epidermis.