| First Author | Rennick DM | Year | 2000 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 278 |
| Issue | 6 | Pages | G829-33 |
| PubMed ID | 10859210 | Mgi Jnum | J:63032 |
| Mgi Id | MGI:1860351 | Doi | 10.1152/ajpgi.2000.278.6.G829 |
| Citation | Rennick DM, et al. (2000) Lessons from genetically engineered animal models. XII. IL-10-deficient (IL-10(-/-) mice and intestinal inflammation. Am J Physiol Gastrointest Liver Physiol 278(6):G829-33 |
| abstractText | Interleukin (IL)-10(-/-) mice spontaneously develop intestinal inflammation characterized by discontinuous transmural lesions affecting the small and large intestine and by dysregulated production of proinflammatory cytokines. The uncontrolled generation of IFN-gamma-producing CD4(+) T cells (Th1 type) has been shown to play a causal role in the development of enterocolitis affecting these mutants. This article discusses studies of IL-10(-/-) mice that have investigated the role of enteric organisms in triggering intestinal disease, the mediators responsible for initiating and maintaining intestinal disease, the role IL-10 plays in the generation and/or function of regulatory cells, and the results of IL-10 therapy in experimental animal models of inflammatory bowel disease (IBD) and human patients with IBD. |
