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

Cell. 1993 Oct 22;75(2):253-61. doi: 10.1016/0092-8674(93)80067-o.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging
  • Animals
  • B-Lymphocytes / physiology
  • Bacterial Infections
  • Colitis, Ulcerative / etiology*
  • Colitis, Ulcerative / genetics
  • Colon / immunology
  • Colon / pathology*
  • Germ-Free Life
  • Homozygote
  • Immunoglobulins / biosynthesis
  • Immunohistochemistry
  • Inflammatory Bowel Diseases / etiology*
  • Inflammatory Bowel Diseases / genetics
  • Interleukin-2 / deficiency*
  • Interleukin-2 / genetics
  • Intestines / cytology
  • Intestines / immunology
  • Mice
  • Mice, Mutant Strains
  • T-Lymphocyte Subsets / physiology
  • Virus Diseases


  • Immunoglobulins
  • Interleukin-2