| First Author | Nakae S | Year | 2002 |
| Journal | Immunity | Volume | 17 |
| Issue | 3 | Pages | 375-87 |
| PubMed ID | 12354389 | Mgi Jnum | J:79127 |
| Mgi Id | MGI:2387256 | Doi | 10.1016/s1074-7613(02)00391-6 |
| Citation | Nakae S, et al. (2002) Antigen-Specific T Cell Sensitization Is Impaired in IL-17-Deficient Mice, Causing Suppression of Allergic Cellular and Humoral Responses. Immunity 17(3):375-387 |
| abstractText | 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. |
