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3 results on '"MESH: B7-2 Antigen"'

1. Antigen targeting to CD11b+ dendritic cells in association with TLR4/TRIF signaling promotes strong CD8+ T cell responses

Author

Catherine Fayolle, Radim Osicka, Sandra Hervas-Stubbs, Marine Oberkampf, Bernard Ryffel, Peter Sebo, Tristan Felix, Gilles Dadaglio, Daniel Ladant, Claude Leclerc, Xiaoming Zhang, Régulation Immunitaire et Vaccinologie, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Universidad de Navarra [Pamplona] (UNAV), Institute of Microbiology of the ASCR, v. v. i. [Prague, Czech Republic], Biochimie des Interactions Macromoléculaires / Biochemistry of Macromolecular Interactions, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), This work was supported by the Ligue Nationale contre le Cancer (Equipe Labellisée 2014), l'Institut National du Cancer/Cancéropole Ile de France, European Union's Seventh Framework Programme Grant 280873, Advanced Immunization Technologies, Czech Science Foundation Grants P302/11/0580 and P302/12/0460, and Banque Privée Européenne., European Project: 280873,EC:FP7:HEALTH,FP7-HEALTH-2011-single-stage,ADITEC(2011), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Dadaglio, Gilles, and Advanced Immunization Technologies - ADITEC - - EC:FP7:HEALTH2011-10-01 - 2016-09-30 - 280873 - VALID

Subjects
MESH: Signal Transduction, [SDV]Life Sciences [q-bio], Interleukin-1beta, Receptor, Interferon alpha-beta, MESH: Mice, Knockout, Bordetella pertussis, MESH: Tyrosine, MESH: Bordetella pertussis, Mice, MESH: Interleukin-1beta, Immunology and Allergy, Cytotoxic T cell, MESH: Animals, Cells, Cultured, Mice, Knockout, CD11b Antigen, biology, MESH: Dendritic Cells, Cell Differentiation, MESH: Toll-Like Receptor 4, 3. Good health, [SDV] Life Sciences [q-bio], medicine.anatomical_structure, B7-1 Antigen, [SDV.IMM]Life Sciences [q-bio]/Immunology, Adenylate Cyclase Toxin, Female, MESH: B7-2 Antigen, MESH: Cells, Cultured, Signal Transduction, MESH: Cell Differentiation, [SDV.IMM] Life Sciences [q-bio]/Immunology, T cell, Immunology, Major histocompatibility complex, MESH: Receptors, Interleukin-1, MESH: CD11b Antigen, Proinflammatory cytokine, Immune system, [SDV.IMM.VAC] Life Sciences [q-bio]/Immunology/Vaccinology, MESH: Mice, Inbred C57BL, medicine, MESH: Receptor, Interferon alpha-beta, Animals, MESH: Mice, MESH: Interferon-beta, Interleukin-6, Tumor Necrosis Factor-alpha, Receptors, Interleukin-1, MESH: Adaptor Proteins, Vesicular Transport, Dendritic Cells, Interferon-beta, cyaA, MESH: Adenylate Cyclase Toxin, MESH: Interleukin-6, Mice, Inbred C57BL, Toll-Like Receptor 4, Adaptor Proteins, Vesicular Transport, TRIF, MESH: Tumor Necrosis Factor-alpha, Cancer research, biology.protein, Tyrosine, MESH: B7-1 Antigen, B7-2 Antigen, [SDV.IMM.VAC]Life Sciences [q-bio]/Immunology/Vaccinology, MESH: Female, MESH: T-Lymphocytes, Cytotoxic, CD8, T-Lymphocytes, Cytotoxic
Abstract

Deciphering the mechanisms that allow the induction of strong immune responses is crucial to developing efficient vaccines against infectious diseases and cancer. Based on the discovery that the adenylate cyclase from Bordetella pertussis binds to the CD11b/CD18 integrin, we developed a highly efficient detoxified adenylate cyclase-based vector (CyaA) capable of delivering a large variety of Ags to the APC. This vector allows the induction of protective and therapeutic immunity against viral and tumoral challenges as well as against transplanted tumors in the absence of any added adjuvant. Two therapeutic vaccine candidates against human papilloma viruses and melanoma have been developed recently, based on the CyaA vector, and are currently in clinical trials. We took advantage of one of these highly purified vaccines, produced under good manufacturing practice–like conditions, to decipher the mechanisms by which CyaA induces immune responses. In this study, we demonstrate that CyaA binds both human and mouse CD11b+ dendritic cells (DCs) and induces their maturation, as shown by the upregulation of costimulatory and MHC molecules and the production of proinflammatory cytokines. Importantly, we show that DCs sense CyaA through the TLR4/Toll/IL-1R domain–containing adapter-inducing IFN-β pathway, independent of the presence of LPS. These findings show that CyaA possesses the intrinsic ability to not only target DCs but also to activate them, leading to the induction of strong immune responses. Overall, this study demonstrates that Ag delivery to CD11b+ DCs in association with TLR4/Toll/IL-1R domain–containing adapter-inducing IFN-β activation is an efficient strategy to promote strong specific CD8+ T cell responses.

Published
2014
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2. Penicillin Binding Proteins as Danger Signals: Meningococcal Penicillin Binding Protein 2 Activates Dendritic Cells through Toll-Like Receptor 4

Author

Gaelle Beriou, Eva Hong, Philippe Blancou, Aude Antignac, Ala-Eddine Deghmane, Meriem El Ghachi, Gaëlle Tilly, Ignacio Anegon, Muhamed-Kheir Taha, Corinne Ruckly, Ivo G. Boneca, Maria Leticia Zarantonelli, Régis Josien, Marcelo Hill, Maria-Cristina Cuturi, Mercedes Segovia, INSERM UMR 643, Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM), Universidad de la República [Montevideo] (UDELAR), Infections Bactériennes Invasives, Institut Pasteur [Paris] (IP), Immuno-Endocrinologie Cellulaire et Moléculaire (IECM), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN)-Ecole Nationale Vétérinaire de Nantes-École nationale vétérinaire, agroalimentaire et de l'alimentation Nantes-Atlantique (ONIRIS), Centre hospitalier universitaire de Nantes (CHU Nantes), Biologie et Génétique de la Paroi bactérienne - Biology and Genetics of Bacterial Cell Wall (BGPB), This work is supported by the Institut Pasteur, Fondation Progreffe and IMBIO. Meriem El Ghachi was supported by a post-doctoral Roux Fellowship (Institut Pasteur). Work in the group of Ivo G. Boneca is supported by an ERC starting Grant (PGNfromSHAPEtoVIR nu 202283)., European Project: 202283,EC:FP7:ERC,ERC-2007-StG,PGNFROMSHAPETOVIR(2008), Universidad de la República [Montevideo] (UCUR), Institut Pasteur [Paris], Ecole Nationale Vétérinaire de Nantes-Université de Nantes (UN)-Institut National de la Recherche Agronomique (INRA), and Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN)-Ecole Nationale Vétérinaire de Nantes

Subjects
Bacterial Diseases, Penicillin binding proteins, Neisseria meningitidis, MESH: Dose-Response Relationship, Drug, Mice, 0302 clinical medicine, penicillin binding protein, polycyclic compounds, MESH: Animals, Immune Response, Cells, Cultured, 0303 health sciences, Toll-like receptor, MESH: Penicillin-Binding Proteins, Multidisciplinary, MESH: Dendritic Cells, MESH: Toll-Like Receptor 4, méningocoque, 3. Good health, Infectious Diseases, Host-Pathogen Interactions, B7-1 Antigen, Medicine, cellule dendritique, Antibody, MESH: B7-2 Antigen, Research Article, MESH: Cells, Cultured, Science, Immune Cells, Immunology, Biology, MESH: Neisseria meningitidis, Microbiology, 03 medical and health sciences, Immune system, In vivo, Animals, Humans, Penicillin-Binding Proteins, MESH: Mice, 030304 developmental biology, CD86, MESH: Humans, Dose-Response Relationship, Drug, Pathogen-associated molecular pattern, MESH: Host-Pathogen Interactions, Immunity, Histocompatibility Antigens Class II, Dendritic Cells, biochemical phenomena, metabolism, and nutrition, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Toll-Like Receptor 4, Immune System, biology.protein, MESH: Histocompatibility Antigens Class II, MESH: B7-1 Antigen, B7-2 Antigen, CD80, 030215 immunology
Abstract

International audience; Neisseria meningitidis is a human pathogen responsible for life-threatening inflammatory diseases. Meningococcal penicillin-binding proteins (PBPs) and particularly PBP2 are involved in bacterial resistance to b-lactams. Here we describe a novel function for PBP2 that activates human and mouse dendritic cells (DC) in a time and dose-dependent manner. PBP2 induces MHC II (LOGEC50 = 4.7 mg/ml60.1), CD80 (LOGEC50 = 4.88 mg/ml60.15) and CD86 (LOGEC50 = 5.36 mg/ml60.1). This effect was abolished when DCs were co-treated with anti-PBP2 antibodies. PBP2-treated DCs displayed enhanced immunogenic properties in vitro and in vivo. Furthermore, proteins co-purified with PBP2 showed no effect on DC maturation. We show through different in vivo and in vitro approaches that this effect is not due to endotoxin contamination. At the mechanistic level, PBP2 induces nuclear localization of p65 NF-kB of 70.765.1% cells versus 1262.6% in untreated DCs and needs TLR4 expression to mature DCs. Immunoprecipitation and blocking experiments showed that PBP2 binds TLR4. In conclusion, we describe a novel function of meningococcal PBP2 as a pathogen associated molecular pattern (PAMP) at the host-pathogen interface that could be recognized by the immune system as a danger signal, promoting the development of immune responses.

Published
2011
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3. Human Macrophages, but Not Dendritic Cells, Are Activated and Produce Alpha/Beta Interferons in Response to Mopeia Virus Infection

Author

Sylvain Baize, Delphine Pannetier, Caroline Faure, Vincent Deubel, Marie-Claude Georges-Courbot, Biologie des Infections Virales Émergentes - Biology of Emerging Viral Infections (UBIVE), Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris] (IP)

Subjects
MESH: Membrane Glycoproteins, Apoptosis, Viral Plaque Assay, medicine.disease_cause, Virus Replication, MESH: CD40 Antigens, MESH: Reverse Transcriptase Polymerase Chain Reaction, Lassa fever, MESH: Antigens, CD, Cells, Cultured, 0303 health sciences, Membrane Glycoproteins, MESH: Dendritic Cells, Reverse Transcriptase Polymerase Chain Reaction, MESH: Antigen-Presenting Cells, MESH: Macrophage Activation, MESH: Arenaviruses, Old World, Intercellular Adhesion Molecule-1, 3. Good health, MESH: Viral Plaque Assay, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, B7-1 Antigen, Tumor necrosis factor alpha, MESH: B7-2 Antigen, MESH: Interferon-alpha, MESH: Cells, Cultured, Immunology, Alpha interferon, Antigen-Presenting Cells, HLA-C Antigens, Biology, Microbiology, Virus, 03 medical and health sciences, Antigens, CD, Virology, medicine, Humans, RNA, Messenger, CD40 Antigens, Antigen-presenting cell, MESH: HLA-A Antigens, 030304 developmental biology, MESH: RNA, Messenger, Arenavirus, MESH: Humans, HLA-A Antigens, MESH: Interferon-beta, 030306 microbiology, Interleukin-6, Tumor Necrosis Factor-alpha, Macrophages, MESH: Apoptosis, MESH: Intercellular Adhesion Molecule-1, MESH: Virus Replication, Interferon-alpha, MESH: Macrophages, Dendritic cell, Dendritic Cells, Interferon-beta, Macrophage Activation, medicine.disease, biology.organism_classification, Molecular biology, MESH: Interleukin-6, MESH: HLA-C Antigens, Lassa virus, HLA-B Antigens, Insect Science, MESH: Tumor Necrosis Factor-alpha, MESH: HLA-B Antigens, Pathogenesis and Immunity, MESH: B7-1 Antigen, B7-2 Antigen, Arenaviruses, Old World
Abstract

Lassa virus (LV) and Mopeia virus (MV) are closely related members of the Arenavirus genus, sharing 75% amino acid sequence identity. However, LV causes hemorrhagic fever in humans and nonhuman primates, whereas MV cannot induce disease. We have previously shown that antigen-presenting cells (APC)—macrophages (MP) and dendritic cells (DC)—sustain high replication rates of LV but are not activated, suggesting that they play a role in the immunosuppression observed in severe cases of Lassa fever. Here, we infected human APC with MV and analyzed the cellular responses induced. MV infection was productive in MP and even more so in DC. Apoptosis was not induced in either cell type. Moreover, unlike DC, MP were early and strongly activated in response to MV, as shown by the increased surface expression of CD86, CD80, CD54, CD40, and HLA-abc and by the production of mRNA encoding alpha interferon (IFN-α), IFN-β, tumor necrosis factor alpha and interleukin-6. In addition, MV-infected MP produced less of the virus than DC, which was related to the fact that these cells secreted IFN-α. Thus, the strong activation of MP is probably a major event in the control of MV infection and may be involved in the induction of an adaptive immune response in infected hosts. These results may explain the difference in pathogenicity between LV and MV.

Published
2004
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