This work was supported by a grant from the Deutsche Forschungsgemeinschaft (Sonderforschungsbereich 280, Teilprojekt C 16) (M.M.) and NIH-PPG-DK44240 (E.H.L.).
Basic Science Review
Genetic and environmental context determines the course of colitis developing in IL–10-deficient mice†
Article first published online: 14 DEC 2006
Copyright © 2002 Crohn's & Colitis Foundation of America, Inc.
Inflammatory Bowel Diseases
Volume 8, Issue 5, pages 347–355, September 2002
How to Cite
Mähler, M. and Leiter, E. H. (2002), Genetic and environmental context determines the course of colitis developing in IL–10-deficient mice. Inflamm Bowel Dis, 8: 347–355. doi: 10.1097/00054725-200209000-00006
- Issue published online: 14 DEC 2006
- Article first published online: 14 DEC 2006
- Manuscript Received: 14 JUN 2002
- Manuscript Accepted: 14 JUN 2002
- Quantitative trait locus;
This review summarizes how interleukin-10 (IL-10)-deficient mice have permitted new insight into the complex interaction between genes and environment underlying pathogenesis of inflammatory bowel disease (IBD). The C57BL/6J strain develops only mild typhlocolitis in response to IL-10 deficiency. In contrast, C3H/HeJBir represents an unrelated inbred strain with high IBD susceptibility. Ability to identify quantitative trait loci segregating for susceptibility when the two IL–10-deficient stocks were intercrossed depended both on genome “context” (F2 versus reciprocal backcrosses) and on the physical environment. These findings are discussed in the context of recent advances in understanding the complex genetic basis for IBD in humans.