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Tytuł :
TL1A and DR3, a TNF family ligand-receptor pair that promotes lymphocyte costimulation, mucosal hyperplasia, and autoimmune inflammation.
Autorzy :
Meylan F; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Richard AC
Siegel RM
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Źródło :
Immunological reviews [Immunol Rev] 2011 Nov; Vol. 244 (1), pp. 188-96.
Typ publikacji :
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
MeSH Terms :
Immunity, Innate*
Receptors, Tumor Necrosis Factor, Member 25/*immunology
Signal Transduction/*immunology
T-Lymphocytes/*immunology
TNF Receptor-Associated Death Domain Protein/*immunology
Tumor Necrosis Factor Ligand Superfamily Member 15/*immunology
Animals ; Asthma/immunology ; Asthma/metabolism ; Autoimmunity ; Cell Proliferation ; Cytokines/biosynthesis ; Cytokines/immunology ; Gene Expression/immunology ; Humans ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/metabolism ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Receptors, Tumor Necrosis Factor, Member 25/genetics ; Receptors, Tumor Necrosis Factor, Member 25/metabolism ; T-Lymphocytes/metabolism ; TNF Receptor-Associated Death Domain Protein/genetics ; TNF Receptor-Associated Death Domain Protein/metabolism ; Tumor Necrosis Factor Ligand Superfamily Member 15/genetics ; Tumor Necrosis Factor Ligand Superfamily Member 15/metabolism
Czasopismo naukowe
Tytuł :
Comparison of gene expression microarray data with count-based RNA measurements informs microarray interpretation.
Autorzy :
Richard, Arianne C (AUTHOR)
Lyons, Paul A (AUTHOR)
Peters, James E (AUTHOR)
Biasci, Daniele (AUTHOR)
Flint, Shaun M (AUTHOR)
Lee, James C (AUTHOR)
McKinney, Eoin F (AUTHOR)
Siegel, Richard M (AUTHOR)
Smith, Kenneth G. C. (AUTHOR)
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Źródło :
BMC Genomics. 2014, Vol. 15 Issue 1, p649-658. 10p. 3 Graphs.
Czasopismo naukowe
Tytuł :
Enhancing the understanding of asthma.
Autorzy :
Vahedi G; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Richard AC; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
O'Shea JJ; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
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Źródło :
Nature immunology [Nat Immunol] 2014 Aug; Vol. 15 (8), pp. 701-3.
Typ publikacji :
Journal Article; Comment
MeSH Terms :
Genetic Predisposition to Disease*
Asthma/*genetics
Asthma/*immunology
Th1 Cells/*immunology
Th2 Cells/*immunology
Female ; Humans ; Male
Czasopismo naukowe
Tytuł :
The TNF-family ligand TL1A and its receptor DR3 promote T cell-mediated allergic immunopathology by enhancing differentiation and pathogenicity of IL-9-producing T cells.
Autorzy :
Richard AC; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Tan C; Experimental Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892;
Hawley ET; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Gomez-Rodriguez J; Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892;
Goswami R; Department of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;
Yang XP; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Cruz AC; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Penumetcha P; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Hayes ET; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Pelletier M; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Gabay O; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Walsh M; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19102;
Ferdinand JR; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO17 1BJ, United Kingdom; and.
Keane-Myers A; Biological Defense Research Directorate, Naval Medical Research Center-Frederick, Fort Detrick, MD 21702.
Choi Y; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19102;
O'Shea JJ; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Al-Shamkhani A; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO17 1BJ, United Kingdom; and.
Kaplan MH; Department of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;
Gery I; Experimental Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892;
Siegel RM; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; .
Meylan F; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
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Źródło :
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2015 Apr 15; Vol. 194 (8), pp. 3567-82. Date of Electronic Publication: 2015 Mar 18.
Typ publikacji :
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms :
Asthma/*immunology
Cell Differentiation/*immunology
Interleukin-9/*immunology
Receptors, Tumor Necrosis Factor, Member 25/*immunology
T-Lymphocytes, Helper-Inducer/*immunology
Tumor Necrosis Factor Ligand Superfamily Member 15/*immunology
Animals ; Asthma/genetics ; Asthma/pathology ; Cell Differentiation/genetics ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-4/genetics ; Interleukin-4/immunology ; Interleukin-9/genetics ; Mice ; Mice, Knockout ; Receptors, Tumor Necrosis Factor, Member 25/genetics ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocytes, Helper-Inducer/pathology ; Tumor Necrosis Factor Ligand Superfamily Member 15/genetics
Czasopismo naukowe
Tytuł :
The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.
Autorzy :
Richard AC; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Ferdinand JR; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Meylan F; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Hayes ET; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Gabay O; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Siegel RM; Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom .
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Źródło :
Journal of leukocyte biology [J Leukoc Biol] 2015 Sep; Vol. 98 (3), pp. 333-45. Date of Electronic Publication: 2015 Jul 17.
Typ publikacji :
Journal Article; Research Support, N.I.H., Intramural; Review
MeSH Terms :
Autoimmune Diseases/*immunology
Receptors, Death Domain/*metabolism
Tumor Necrosis Factor Ligand Superfamily Member 15/*metabolism
Animals ; Autoimmune Diseases/pathology ; Disease Models, Animal ; Humans ; Lymphocyte Activation/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Czasopismo naukowe
Tytuł :
Correction: The TNF-Family Ligand TL1A and Its Receptor DR3 Promote T Cell-Mediated Allergic Immunopathology by Enhancing Differentiation and Pathogenicity of IL-9-Producing T Cells.
Autorzy :
Richard AC
Tan C
Hawley ET
Gomez-Rodriguez J
Goswami R
Yang XP
Cruz AC
Penumetcha P
Hayes ET
Pelletier M
Gabay O
Walsh M
Ferdinand JR
Keane-Myers A
Choi Y
O'Shea JJ
Al-Shamkhani A
Kaplan MH
Gery I
Siegel RM
Meylan F
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Źródło :
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2015 Dec 15; Vol. 195 (12), pp. 5839-40.
Typ publikacji :
Published Erratum
Tytuł :
Targeted genomic analysis reveals widespread autoimmune disease association with regulatory variants in the TNF superfamily cytokine signalling network.
Autorzy :
Richard AC; Department of Medicine and Cambridge Institute for Medical Research, The University of Cambridge, Box 139, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.; Autoimmunity Branch, National Institute for Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Peters JE; Department of Medicine and Cambridge Institute for Medical Research, The University of Cambridge, Box 139, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Lee JC; Department of Medicine and Cambridge Institute for Medical Research, The University of Cambridge, Box 139, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Vahedi G; Department of Genetics, Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Schäffer AA; Computational Biology Branch, National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD, 20894, USA.
Siegel RM; Autoimmunity Branch, National Institute for Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Lyons PA; Department of Medicine and Cambridge Institute for Medical Research, The University of Cambridge, Box 139, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
Smith KG; Department of Medicine and Cambridge Institute for Medical Research, The University of Cambridge, Box 139, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK. .
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Źródło :
Genome medicine [Genome Med] 2016 Jul 19; Vol. 8 (1), pp. 76. Date of Electronic Publication: 2016 Jul 19.
Typ publikacji :
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms :
Genetic Predisposition to Disease*
Quantitative Trait Loci*
Autoimmune Diseases/*genetics
Hereditary Autoinflammatory Diseases/*genetics
Receptors, Tumor Necrosis Factor/*genetics
Tumor Necrosis Factor-alpha/*genetics
Alleles ; Autoimmune Diseases/diagnosis ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Chromatin/chemistry ; Chromatin/immunology ; Gene Expression Regulation ; Gene Regulatory Networks ; Genome, Human ; Genome-Wide Association Study ; Hereditary Autoinflammatory Diseases/diagnosis ; Hereditary Autoinflammatory Diseases/immunology ; Hereditary Autoinflammatory Diseases/pathology ; Humans ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/pathology ; Protein Isoforms/genetics ; Protein Isoforms/immunology ; Receptors, Tumor Necrosis Factor/immunology ; Risk ; Signal Transduction ; Tumor Necrosis Factor-alpha/immunology
Czasopismo naukowe
Tytuł :
Testing for differential abundance in mass cytometry data.
Autorzy :
Lun ATL; Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Richard AC; Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.; Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
Marioni JC; Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.; EMBL European Bioinformatics Institute, Wellcome Genome Campus, Cambridge, UK.; Wellcome Trust Sanger Institute, Wellcome Genome Campus, Cambridge, UK.
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Źródło :
Nature methods [Nat Methods] 2017 Jul; Vol. 14 (7), pp. 707-709. Date of Electronic Publication: 2017 May 15.
Typ publikacji :
Journal Article
MeSH Terms :
Software*
Flow Cytometry/*methods
Image Processing, Computer-Assisted/*methods
Computer Simulation
Czasopismo naukowe
Tytuł :
Cleavage of TL1A Differentially Regulates Its Effects on Innate and Adaptive Immune Cells.
Autorzy :
Ferdinand JR; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892.; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO16 6YD, United Kingdom.
Richard AC; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892.; Cambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom; and.; Department of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Meylan F; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892.
Al-Shamkhani A; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO16 6YD, United Kingdom.
Siegel RM; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; .
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Źródło :
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2018 Feb 15; Vol. 200 (4), pp. 1360-1369. Date of Electronic Publication: 2018 Jan 15.
Typ publikacji :
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
MeSH Terms :
Adaptive Immunity/*immunology
Immunity, Innate/*immunology
Lymphocyte Activation/*immunology
Tumor Necrosis Factor Ligand Superfamily Member 15/*immunology
Tumor Necrosis Factor Ligand Superfamily Member 15/*metabolism
Animals ; Mice ; Mice, Transgenic ; T-Lymphocytes/immunology
Czasopismo naukowe

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