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

来自 dx.doi.org

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作者：

Benjamin Sadlack *，Hartmut Merz †，Hubert Schorle *，Anneliese Schimpl *，Alfred C. Feller †，Ivan Horak *

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摘要：

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.

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关键词：

Intestines Colon B-Lymphocytes T-Lymphocyte Subsets Animals Mice Mice, Mutant Strains Bacterial Infections Virus Diseases Colitis, Ulcerative