| First Author | Madsen L | Year | 1999 |
| Journal | Proc Natl Acad Sci U S A | Volume | 96 |
| Issue | 18 | Pages | 10338-43 |
| PubMed ID | 10468609 | Mgi Jnum | J:57484 |
| Mgi Id | MGI:1344858 | Doi | 10.1073/pnas.96.18.10338 |
| Citation | Madsen L, et al. (1999) Mice lacking all conventional MHC class II genes. Proc Natl Acad Sci U S A 96(18):10338-43 |
| abstractText | MHC class II (MHC-II) molecules play a central role in the selection of the T cell repertoire, in the establishment and regulation of the adaptive immune response, and in autoimmune deviation. We have generated knockout mice lacking all four of the classical murine MHC-II genes (MHCII(Delta/Delta) mice), via a large (80-kilobase) deletion of the entire class II region that was engineered by homologous recombination and Cre recombinase-mediated excision. These mice feature immune system perturbations like those of Aalpha and Abeta knockout animals, notably a dearth of CD4(+) lymphocytes in the thymus and spleen. No new anatomical or physiological abnormalities were observed in MHCII(Delta/Delta) mice. Because these animals are devoid of all classical MHC-II chains, even unpaired chains, they make excellent recipients for MHC-II transgenes from other species, avoiding the problem of interspecies cross-pairing of MHC-II chains. Therefore, they should be invaluable for engineering 'humanized' mouse models of human MHC-II-associated autoimmune disorders. |
