| First Author | Sadlack B | Year | 1993 |
| Journal | Cell | Volume | 75 |
| Issue | 2 | Pages | 253-61 |
| PubMed ID | 8402910 | Mgi Jnum | J:15223 |
| Mgi Id | MGI:63352 | Doi | 10.1016/0092-8674(93)80067-o |
| Citation | Sadlack B, et al. (1993) Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene [see comments]. Cell 75(2):253-61 |
| abstractText | 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 the remaining mice, 100% develop an inflammatory bowel disease with striking clinical and histological similarity to ulcerative colitis in humans. The alterations of the immune system are characterized by a high number of activated T and B cells, elevated immunoglobulin secretion, anti-colon antibodies, and aberrant expression of class II major histocompatibility complex molecules. The data provide evidence for a primary role of the immune system in the etiology of ulcerative colitis and strongly suggest that the disease results from an abnormal immune response to a normal antigenic stimulus. |
