ULCERATIVE COLITIS-LIKE DISEASE IN MICE WITH A DISRUPTED INTERLEUKIN-2 GENE

Mice deficient for interleukin-2 develop normally during the first 3-4 weeks of age. However, later on they become severely compromised, and about 50% of the animals die between 4 and 9 weeks after birth. Of th e remaining mice, 100% develop an inflammatory bowel disease with stri king clinical and histological similarity to ulcerative colitis in hum ans. The alterations of the immune system are characterized by a high number of activated T and B cells, elevated immunoglobin secretion, an ti-colon antibodies, and aberrant expression of class II major histoco mpatibility complex molecules. The data provide evidence for a primary role of the immune system in the etiology of ulcerative colitis and s trongly suggest that the disease results from an abnormal immune respo nse to a normal antigenic stimulus.