Your browser doesn't support javascript.
loading
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.
Richard, Arianne C; Tan, Cuiyan; Hawley, Eric T; Gomez-Rodriguez, Julio; Goswami, Ritobrata; Yang, Xiang-Ping; Cruz, Anthony C; Penumetcha, Pallavi; Hayes, Erika T; Pelletier, Martin; Gabay, Odile; Walsh, Matthew; Ferdinand, John R; Keane-Myers, Andrea; Choi, Yongwon; O'Shea, John J; Al-Shamkhani, Aymen; Kaplan, Mark H; Gery, Igal; Siegel, Richard M; Meylan, Françoise.
Afiliação
  • 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; rsiegel@nih.gov.
  • Meylan F; Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
J Immunol ; 194(8): 3567-82, 2015 Apr 15.
Article em En | MEDLINE | ID: mdl-25786692
Assuntos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Diferenciação Celular / Interleucina-9 / Linfócitos T Auxiliares-Indutores / Membro 15 da Superfamília de Ligantes de Fatores de Necrose Tumoral / Membro 25 de Receptores de Fatores de Necrose Tumoral Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: J Immunol Ano de publicação: 2015 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Diferenciação Celular / Interleucina-9 / Linfócitos T Auxiliares-Indutores / Membro 15 da Superfamília de Ligantes de Fatores de Necrose Tumoral / Membro 25 de Receptores de Fatores de Necrose Tumoral Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: J Immunol Ano de publicação: 2015 Tipo de documento: Article