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Am J Physiol Gastrointest Liver Physiol 278: G829-G833, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 6, G829-G833, June 2000

THEMES
Lessons From Genetically Engineered Animal Models
XII. IL-10-deficient (IL-10minus /minus ) mice and intestinal inflammation*

Donna M. Rennick and Madeline M. Fort

DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, California 94304

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.

interleukin; counterregulation by IL-10; proinflammatory cytokines; Th1-mediated intestinal disease; IL-10 therapy

* Twelfth in a series of invited articles on Lessons From Genetically Engineered Animal Models.




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