Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene
B Sadlack, H Merz, H Schorle, A Schimpl, AC Feller… - Cell, 1993 - cell.com
B Sadlack, H Merz, H Schorle, A Schimpl, AC Feller, I Horak
Cell, 1993•cell.comMice 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 …
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 …
Summary
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 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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