Oer the past several years, a variety of animal models of inflammatory bowel disease (IBD) have been developed and investigated, with the ultimate goal of understanding the causes of Crohn’s disease (CD) and ulcerative colitis (UC).^1,2 Unfortunately, thus far no single animal model recapitulates all of the pathogenic and clinical features of human IBD, which has impeded our progress towards an understanding of the precise causes of these devastating diseases. Nevertheless, each animal model has provided us with a unique opportunity to advance our understanding of the mechanisms underlying initiation and perpetuation of chronic intestinal inflammation. This has allowed identification of novel targets in the disease process for potential therapeutic intervention. For instance, the explosion in the number of animal models of colitis based on gene deletion or overexpression has underlined the importance of cytokine gene products in gut immune regulation.³ Perhaps one of the best examples in this category is the interleukin (IL)-10 deficient mouse, which develops chronic enteritis, the characteristics of which are similar to human IBD.⁴ Despite the fact that no genetic or immunological abnormalities of the IL-10 pathway have been demonstrated in patients with IBD to date, this model has facilitated the development of therapeutic strategies based on administration of anti-inflammatory cytokines⁵ or delivery of regulatory T cells with anti-inflammatory activities.⁶

The …