| First Author | Marguerat S | Year | 1999 |
| Journal | J Immunol | Volume | 163 |
| Issue | 7 | Pages | 4033-40 |
| PubMed ID | 10491007 | Mgi Jnum | J:119199 |
| Mgi Id | MGI:3701532 | Doi | 10.4049/jimmunol.163.7.4033 |
| Citation | Marguerat S, et al. (1999) Protection from radiation-induced colitis requires MHC class II antigen expression by cells of hemopoietic origin. J Immunol 163(7):4033-40 |
| abstractText | Ulcerative colitis, an inflammatory bowel disease, is believed to result from a breakdown of dominant tolerance mechanisms that normally control intestinal immunity. Although CD4+ T lymphocyte subpopulations and expression of MHC class II molecules have been shown to play a role in the pathogenesis of the disease, the nature of the responsible mechanisms remains unclear. In this paper we describe a novel mouse model for inflammatory bowel disease, radiation-induced colitis, that occurs with complete penetrance 6-8 wk postinduction. A combination of high dose gamma-irradiation and lack of MHC class II expression on cells of hemopoietic origin results in development of colitis in C57BL/6 mice. Because of its versatility (due to susceptibility of mice of the widely genetically manipulated C57BL/6 background), high reproducibility, and 100% penetrance, radiation-induced colitis will be a useful mouse model for colitis and a significant tool to study dominant immunological tolerance mechanisms. Moreover, our data imply that tolerization to enteric Ags requires MHC class II mediated presentation by APC of hemopoietic origin. |
