Search

Your search keyword '"MESH: CD40 Antigens"' showing total 3 results
Start Over Descriptor "MESH: CD40 Antigens"
3 results on '"MESH: CD40 Antigens"'

1. Inhibitory IgG Receptor-Expressing Cells: The Must-Have Accessory for Anti-CD40 Immunomodulatory mAb Efficacy

Author

Pierre Bruhns, Jean-Luc Teillaud, Martin, Marie, Anticorps en thérapie et pathologie - Antibodies in Therapy and Pathology, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), École Pratique des Hautes Études (EPHE), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP)

Subjects
0301 basic medicine, Cancer Research, [SDV.IMM] Life Sciences [q-bio]/Immunology, medicine.drug_class, MESH: Receptors, IgG, Biology, Pharmacology, Monoclonal antibody, Inhibitory postsynaptic potential, Article, MESH: Antibodies, Monoclonal, 03 medical and health sciences, 0302 clinical medicine, MESH: CD40 Antigens, medicine, Animals, Humans, MESH: Animals, Anti cd40, CD40 Antigens, Receptor, MESH: Humans, CD40, Receptors, IgG, Antibodies, Monoclonal, Cell Biology, Treatment efficacy, 3. Good health, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Immunology, Cancer cell, biology.protein, [SDV.IMM]Life Sciences [q-bio]/Immunology, Antibody
Abstract

While engagement of the inhibitory Fcγ-Receptor (FcγR) IIB is an absolute requirement for in vivo antitumor activity of agonistic mouse anti-CD40 monoclonal antibodies (mAbs), a similar requirement for human mAbs has been disputed. By using a mouse model humanized for its FcγRs and CD40, we revealed that FcγRIIB-engagement is essential for the activity of the human CD40 mAbs, while engagement of the activating FcγRIIA inhibits this activity. By engineering Fc variants with selective enhanced binding to FcγRIIB, but not to FcγRIIA, significantly improved antitumor immunity was observed. These findings highlight the necessity of optimizing the Fc domain for this class of therapeutic antibodies by using appropriate pre-clinical models that accurately reflect the unique affinities and cellular expression of human FcγR.

Published
2016
Full Text
View/download PDF

2. 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
Full Text
View/download PDF

3. An ACT1 Mutation Selectively Abolishes Interleukin-17 Responses in Humans with Chronic Mucocutaneous Candidiasis

Author

Michel Rybojad, Vincent Pedergnana, Bertrand Boisson, Jean-Laurent Casanova, Ling Wu, Claire Fieschi, Laurent Abel, Capucine Picard, Xiaoxia Li, Aziz Belkadi, Chenhui Wang, Sophie Cypowyj, Anne Puel, St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller University [New York], Cleveland Clinic, Génétique Humaine des Maladies Infectieuses (Inserm U980), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Service de Dermatologie [AP-HP Hôpital Saint-Louis], Hopital Saint-Louis [AP-HP] (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service d'Immunopathologie [Hôpital Saint-Louis, Paris], Université Paris Diderot - Paris 7 (UPD7)-Hopital Saint-Louis [AP-HP] (AP-HP), Université Paris Diderot - Paris 7 (UPD7), and Herrada, Anthony

Subjects
Male, T-Lymphocytes, MESH: Interleukin-17, [SDV]Life Sciences [q-bio], MESH: Amino Acid Sequence, MESH: Heat-Shock Proteins, medicine.disease_cause, MESH: Receptors, Interleukin-17, MESH: Protein Structure, Tertiary, 0302 clinical medicine, MESH: CD40 Antigens, Immunology and Allergy, Missense mutation, Chronic mucocutaneous candidiasis, MESH: Candidiasis, Chronic Mucocutaneous, Receptor, Heat-Shock Proteins, 0303 health sciences, Mutation, Receptors, Interleukin-17, MESH: Protein Multimerization, Candidiasis, Chronic Mucocutaneous, Homozygote, Interleukin-17, Tumor Necrosis Factor Receptor-Associated Peptides and Proteins, Pedigree, [SDV] Life Sciences [q-bio], Infectious Diseases, Female, Tumor necrosis factor alpha, MESH: Immunity, Innate, Interleukin 17, MESH: Homozygote, Adult, MESH: Pedigree, Molecular Sequence Data, Immunology, Mucocutaneous zone, Mutation, Missense, macromolecular substances, Biology, MESH: Tumor Necrosis Factor Receptor-Associated Peptides and Proteins, Article, 03 medical and health sciences, Heat shock protein, medicine, Humans, Amino Acid Sequence, CD40 Antigens, Immunity, Mucosal, Adaptor Proteins, Signal Transducing, 030304 developmental biology, MESH: Adaptor Proteins, Signal Transducing, MESH: Mutation, Missense, MESH: Molecular Sequence Data, MESH: Humans, Siblings, MESH: Adult, Fibroblasts, medicine.disease, Immunity, Innate, MESH: Male, Protein Structure, Tertiary, MESH: Siblings, MESH: T-Lymphocytes, MESH: Fibroblasts, MESH: Immunity, Mucosal, Protein Multimerization, MESH: Female, 030215 immunology
Abstract

International audience; Patients with inborn errors of interleukin-17F (IL-17F) or IL-17RA display chronic mucocutaneous candidiasis (CMC). We report a biallelic missense mutation (T536I) in the adaptor molecule ACT1 in two siblings with CMC. The mutation, located in the SEFIR domain, abolished the homotypic interaction of ACT1 with IL-17 receptors, with no effect on homodimerization. The patients' fibroblasts failed to respond to IL-17A and IL-17F, and their T cells to IL-17E. By contrast, healthy individuals homozygous for the common variant D10N, located in the ACT1 tumor necrosis factor receptor-associated factor-interacting domain and previously associated with psoriasis, had impaired, but not abolished, responses to IL-17 cytokines. SEFIR-independent interactions of ACT1 with other proteins, such as CD40, heat shock protein 70 (HSP70) and HSP90, were not affected by the T536I mutation. Overall, human IL-17A and IL-17F depend on ACT1 to mediate protective mucocutaneous immunity. Moreover, other ACT1-dependent IL-17 cytokines seem to be largely redundant in host defense.

Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results