Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene.
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.
Sadlack
B
B
Institute of Virology and Immunobiology, University of Würzburg, Federal Republic of Germany.
Merz
H
H
Schorle
H
H
Schimpl
A
A
Feller
A C
AC
Horak
I
I
D000375:Aging; D000818:Animals; D001402:B-Lymphocytes / Q000502:physiology; D001424:Bacterial Infections; D003093:Colitis, Ulcerative / Q000209:etiology* / Q000235:genetics; D003106:Colon / Q000276:immunology / Q000473:pathology*; D005856:Germ-Free Life; D006720:Homozygote; D007136:Immunoglobulins / Q000096:biosynthesis; D007150:Immunohistochemistry; D015212:Inflammatory Bowel Diseases / Q000209:etiology* / Q000235:genetics; D007376:Interleukin-2 / Q000172:deficiency* / Q000235:genetics; D007422:Intestines / Q000166:cytology / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains; D016176:T-Lymphocyte Subsets / Q000502:physiology; D014777:Virus Diseases
D007136:Immunoglobulins; D007376:Interleukin-2