| First Author | Guerder S | Year | 1998 |
| Journal | J Immunol | Volume | 161 |
| Issue | 5 | Pages | 2128-40 |
| PubMed ID | 9725204 | Mgi Jnum | J:93555 |
| Mgi Id | MGI:3057302 | Doi | 10.4049/jimmunol.161.5.2128 |
| Citation | Guerder S, et al. (1998) Autoimmunity without diabetes in transgenic mice expressing beta cell-specific CD86, but not CD80: parameters that trigger progression to diabetes. J Immunol 161(5):2128-40 |
| abstractText | To define more clearly the roles of CD80 (RIP-CD80) and CD86 (RIP-CD86) in the activation of autoreactive T cells in vivo, we generated transgenic mice expressing either or both costimulatory molecules on the beta cells of the pancreas. While RIP-CD80 mice do not show any sign of autoimmunity, at the age of 7 mo RIP-CD86 transgenic mice develop a lymphoid infiltrate with both IFN-gamma- and IL-4-positive cells in the vicinity of the islets; these mice, however, never progress to diabetes. This fundamental difference in the ability of CD80 and CD86 to activate self-reactive T cells in vivo is, however, obliterated when the level of TCR signaling is increased by either TNF-alpha or transgenic MHC class II expression. These results support the suggestion that CD80 and CD86 mainly differ at the level of the intensity of the signals they deliver. |
