2-4-dinitrofluorobenzene-sulfonic-acid and Bronchial-Hyperreactivity

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.

Topics: Acute Disease; Animals; Antibody Formation; B-Lymphocytes; Bronchial Hyperreactivity; CD4-Positive T-Lymphocytes; Cells, Cultured; Coculture Techniques; Dendritic Cells; Dermatitis, Allergic Contact; Dinitrofluorobenzene; Female; Graft vs Host Reaction; Haptens; Hypersensitivity, Delayed; Immunity, Cellular; Interleukin-17; Lymphocyte Activation; Lymphocyte Cooperation; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; Mitogens; Models, Animal; Nickel; Picryl Chloride; Specific Pathogen-Free Organisms; Spleen; T-Lymphocyte Subsets; Tumor Necrosis Factor-alpha