| First Author | Siegmund K | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 6 | Pages | 3452-61 |
| PubMed ID | 21289301 | Mgi Jnum | J:169779 |
| Mgi Id | MGI:4942232 | Doi | 10.4049/jimmunol.1003491 |
| Citation | Siegmund K, et al. (2011) Coronin 1-mediated naive T cell survival is essential for the development of autoimmune encephalomyelitis. J Immunol 186(6):3452-61 |
| abstractText | Autoimmune encephalomyelitis is a disease of the CNS that can develop when an initial peripheral inflammatory stimulus is followed by infiltration and reactivation of T lymphocytes in the CNS. We report a crucial role for coronin 1, which is essential for maintenance of the naive T cell pool, for the development of murine experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. In the absence of coronin 1, immunization with myelin oligoglycoprotein (MOG(35-55)) peptide largely failed to induce EAE symptoms, despite normal mobilization of leukocyte subsets in the blood, as well as effector cytokine expression comparable with wild-type T cells on polyclonal stimulation. Susceptibility of coronin 1-deficient mice to EAE induction was restored by transfer of wild-type CD4(+) T cells, suggesting that the observed resistance of coronin 1-deficient mice to EAE development is T cell intrinsic. Importantly, although coronin 1-deficient regulatory T cells (Tregs) showed a suppressor activity comparable with wild-type Tregs, Treg depletion failed to restore EAE development in coronin 1-deficient animals. These results suggest a hitherto unrecognized role of naive T cells in the development of autoimmune encephalomyelitis and reveal coronin 1 as a crucial modulator of EAE induction. |
