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Cell. 1993 Oct 22;75(2):253-61.

Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene.

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Institute of Virology and Immunobiology, University of W├╝rzburg, Federal Republic of Germany.


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.

[Indexed for MEDLINE]

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