| First Author | Jevnikar AM | Year | 1994 |
| Journal | J Exp Med | Volume | 179 |
| Issue | 4 | Pages | 1137-43 |
| PubMed ID | 7908320 | Mgi Jnum | J:17444 |
| Mgi Id | MGI:65482 | Doi | 10.1084/jem.179.4.1137 |
| Citation | Jevnikar AM, et al. (1994) Prevention of nephritis in major histocompatibility complex class II-deficient MRL-lpr mice. J Exp Med 179(4):1137-43 |
| abstractText | MRL-lpr mice develop aggressive autoimmune kidney disease associated with increased or de novo renal expression of major histocompatibility complex (MHC) class II molecules and a massive systemic expansion of CD4-CD- double negative (DN) T cells. Whereas non-MHC linked genes can have a profound effect on the development of nephritis, lymphadenopathy, and anti-DNA antibody production in MRL-lpr mice, the role of MHC molecules has not been unequivocally established. To study the role of MHC class II in this murine model of systemic lupus erythematosis, class II-deficient MRL-lpr mice (MRL-lpr -/-) were created. MRL-lpr -/- mice developed lymphadenopathy but not autoimmune renal disease or autoantibodies. This study demonstrates that class II expression is critical for the development of autoaggressive CD4+ T cells involved in autoimmune nephritis and clearly dissociates DN T cell expansion from autoimmune disease initiation. |
