| First Author | Rudolph U | Year | 1995 |
| Journal | J Clin Immunol | Volume | 15 |
| Issue | 6 Suppl | Pages | 101S-105S |
| PubMed ID | 8613481 | Mgi Jnum | J:30507 |
| Mgi Id | MGI:78016 | Doi | 10.1007/BF01540899 |
| Citation | Rudolph U, et al. (1995) Gi2 alpha protein deficiency: a model of inflammatory bowel disease. J Clin Immunol 15(6 Suppl):101S-105S |
| abstractText | Mice deficient for the G protein subunit Gi2 alpha were obtained by gene targeting. They displayed a growth retardation that was apparent at 6 weeks of age. They subsequently developed diffuse colitis with clinical and histopathological features closely resembling those of ulcerative colitis in humans. Seven of 20 Gi2 alpha-deficient mice with colitis also developed adenocarcinomas of the colon. Gi2 alpha-deficient thymocytes displayed two- to fourfold increases in mature CD4+8- and CD4-8+ phenotypes, an approximately threefold increase in high-intensity CD3 staining and enhanced proliferative responses to T-cell receptor stimuli. Stimulation of Gi 2 alpha-deficient peripheral T cells induced a hyperresponsive profile of interleukin-2, tumour necrosis factor, and interferon-gamma production, which may reflect a heightened response of primed cells or a defective negative regulation. We suggest that Gi 2 alpha-deficient mice may represent a useful animal model for dissecting the pathomechanisms of inflammatory bowel disease and also for the development of novel therapeutic strategies. |
