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

Abstract:

: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.

journal_name

Cell

journal_title

Cell

authors

Sadlack B,Merz H,Schorle H,Schimpl A,Feller AC,Horak I

doi

10.1016/0092-8674(93)80067-o

subject

Has Abstract

pub_date

1993-10-22 00:00:00

pages

253-61

issue

2

eissn

0092-8674

issn

1097-4172

pii

0092-8674(93)80067-O

journal_volume

75

pub_type

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