Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene
1993; Cell Press; Volume: 75; Issue: 2 Linguagem: Inglês
10.1016/0092-8674(93)80067-o
ISSN1097-4172
AutoresBenjamin Sadlack, Hartmut Merz, Hubert Schorle, Anneliese Schimpl, Alfred C. Feller, Ivan D. Horak,
Tópico(s)Immune Response and Inflammation
ResumoMice 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 immunoglobin 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.
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