An inflammatory bowel disease (IBD) syndrome/ Crohn’s disease model, caused by the deregulated overexpression of TNF by knock-in of a murine TNFÄÁRE gene. This model is characterized by gastrointenstinal inflammation, as well as rheumatoid arthritis like pathology by 7 weeks of age. It is unique in that in a single study the efficacy of a drug can be assessed for both arthritis and inflammatory bowel disease syndrome. Additionally, it can be used to test the effectiveness of IBD directed therapeutics by using the rheumatoid arthritis phenotype as a control.(view the original article).
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TNF+/+ |
TNFÄARE
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TNF+/+ control at 7 weeks. The villus height and inflammatory component are Normal.
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TNFÄARE/ÄARE homozygote at 7 weeks. Villi are blunted and distorted, with a marked inflammatory infiltrate composed of lymphocytes, plasma cells, scattered neutrophils, and collections of submucosal histiocytes forming rudimentary Granulomata.
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TNF+/+ |
TNFÄARE
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Histologic examination of ankle joints. Formation of the inflammatory pannus and areas of cartilage and bone erosion are evident in the TNFÄARE
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Inflammatory Bowel Disease
