Dm. Rennick et Mm. Fort, Lessons from genetically engineered animal models - XII. IL-10-deficient (IL-10(-/-)) mice and intestinal inflammation, AM J P-GAST, 278(6), 2000, pp. G829-G833
Citations number
31
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
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 ty
pe) has been shown to play a causal role in the development of enterocoliti
s affecting these mutants. This article discusses studies of IL-10(-/-) mic
e that have investigated the role of enteric organisms in triggering intest
inal disease, the mediators responsible for initiating and maintaining inte
stinal disease, the role IL-10 plays in the generation and/or function of r
egulatory cells, and the results of IL-10 therapy in experimental animal mo
dels of inflammatory bowel disease (IBD) and human patients with IBD.