| First Author | Matsuki T | Year | 2006 |
| Journal | Int Immunol | Volume | 18 |
| Issue | 2 | Pages | 399-407 |
| PubMed ID | 16415102 | Mgi Jnum | J:106619 |
| Mgi Id | MGI:3619104 | Doi | 10.1093/intimm/dxh379 |
| Citation | Matsuki T, et al. (2006) Abnormal T cell activation caused by the imbalance of the IL-1/IL-1R antagonist system is responsible for the development of experimental autoimmune encephalomyelitis. Int Immunol 18(2):399-407 |
| abstractText | IL-1 is a pro-inflammatory cytokine that plays an important role in inflammation and host responses to infection. We have previously shown that imbalances in the IL-1 and IL-1R antagonist (IL-1Ra) system cause the development of inflammatory diseases. To explore the role of the IL-1/IL-1Ra system in autoimmune disease, we analyzed myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in mice bearing targeted disruptions of the IL-1alpha, IL-1beta, IL-1alpha and IL-1beta (IL-1) or IL-1Ra genes. IL-1alpha/beta double-deficient (IL-1(-/-)) mice exhibited significant resistance to EAE induction with a significant reduction in disease severity, while IL-1alpha(-/-) or IL-1beta(-/-) mice developed EAE in a manner similar to wild-type mice. IL-1Ra(-/-) mice also developed MOG-induced EAE normally with pertussis toxin (PTx) administration. In contrast to wild-type mice, however, these mice were highly susceptible to EAE induction in the absence of PTx administration. We found that both IFN-gamma and IL-17 production and proliferation were reduced in IL-1(-/-) T cells upon stimulation with MOG, while IFN-gamma, IL-17 and tumor necrosis factor-alpha production and proliferation were enhanced in IL-1Ra(-/-) T cells. These observations suggest that the IL-1/IL-1Ra system is crucial for auto-antigen-specific T cell induction and contributes to the development of EAE. |
