Antigen-specific T Cell Sensitization Is Impaired in IL-17-deficient Mice, Causing Suppression of Allergic Cellular and Humoral Responses

Immunity. 2002 Sep;17(3):375-87. doi: 10.1016/s1074-7613(02)00391-6.

Abstract

Interleukin-17 (IL-17) is a proinflammatory cytokine produced by T cells. The involvement of IL-17 in human diseases has been suspected because of its detection in sera from asthmatic patients and synovial fluids from arthritic patients. In this study, we generated IL-17-deficient mice and investigated the role of IL-17 in various disease models. We found that contact, delayed-type, and airway hypersensitivity responses, as well as T-dependent antibody production, were significantly reduced in the mutant mice, while IL-17 deficiency of donor T cells did not affect acute graft-versus-host reaction. The results suggest that impaired responses were caused by the defects of allergen-specific T cell activation. Our findings indicate that IL-17 plays an important role in activating T cells in allergen-specific T cell-mediated immune responses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Animals
  • Antibody Formation
  • B-Lymphocytes / immunology
  • Bronchial Hyperreactivity / genetics
  • Bronchial Hyperreactivity / immunology*
  • CD4-Positive T-Lymphocytes / immunology
  • Cells, Cultured / immunology
  • Coculture Techniques
  • Dendritic Cells / immunology
  • Dermatitis, Allergic Contact / genetics
  • Dermatitis, Allergic Contact / immunology
  • Dinitrofluorobenzene / analogs & derivatives*
  • Dinitrofluorobenzene / immunology
  • Female
  • Graft vs Host Reaction / immunology*
  • Haptens / immunology
  • Hypersensitivity, Delayed / genetics
  • Hypersensitivity, Delayed / immunology*
  • Immunity, Cellular
  • Interleukin-17 / deficiency
  • Interleukin-17 / genetics
  • Interleukin-17 / physiology*
  • Lymphocyte Activation / drug effects
  • Lymphocyte Cooperation
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogens / pharmacology
  • Models, Animal
  • Nickel / immunology
  • Picryl Chloride / immunology
  • Specific Pathogen-Free Organisms
  • Spleen / transplantation
  • T-Lymphocyte Subsets / immunology*
  • Tumor Necrosis Factor-alpha / deficiency
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Haptens
  • Interleukin-17
  • Mitogens
  • Tumor Necrosis Factor-alpha
  • 2,4-dinitrofluorobenzene sulfonic acid
  • Nickel
  • Dinitrofluorobenzene
  • Picryl Chloride