The SAMP1/Yit mouse: another step closer to modeling human inflammatory bowel disease

, Kosiewicz andher colleagues (1) provide valuable clin-ical data and the first systematicimmunologic study of the SAMP1/Yitmouse, a murine model of sponta-neous gastrointestinal inflammationthat bears remarkable similarity tohuman Crohn’s disease. The mousestrain used has its origin in strainsdeveloped in the early 1980s for a verydifferent purpose. Hoping to study thegenetics of aging, Takeda et al. inter-bred AKR mice to generate senescence-prone or senescence-resistant sublines,including the short-lived strain SAMP1(2). In the 1990s, Matsumoto et al.established a new subline of theSAMP1 mouse with spontaneous skinulcerations (3). The SAMP1/Yit strain,which arose from SAMP1, no longerundergoes accelerated senescence, butit exhibits the novel phenotype ofspontaneous intestinal inflammation.Genetic analysis in the present reportshows that approximately 40% of thepolymorphic alleles in the SAMP1/Yitgenome differ from the original AKRstrain, indicating that genetic materialfrom one or more other strains wasintroduced into this line at some pointin the SAMP1/Yit pedigree. Regardlessof the origin of these unexpected alle-les, SAMP1/Yit is now an inbred strainof great promise for the study ofCrohn’s disease pathogenesis.As described initially by Matsumotoet al. (3), the intestinal lesions in theSAMP1/Yit mouse strain consist of dis-continuous inflammatory lesionsoccurring mainly in the terminal ileum,and to a lesser extent the cecum, whichare more or less similar to those occur-ring in Crohn’s disease. These lesionsconsist of an extensive infiltration ofCD3