Lessons from genetically engineered animal models. XII. IL-10-deficient (IL-10(-/-) mice and intestinal inflammation.
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.
Rennick
D M
DM
DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, California 94304, USA.
Fort
M M
MM
D000818:Animals; D003093:Colitis, Ulcerative / Q000503:physiopathology*; D003424:Crohn Disease / Q000503:physiopathology*; D004195:Disease Models, Animal; D005818:Genetic Engineering; D006801:Humans; D016753:Interleukin-10 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout / Q000235:genetics
D016753:Interleukin-10