ULCERATIVE COLITIS-LIKE DISEASE IN MICE WITH A DISRUPTED INTERLEUKIN-2 GENE

被引：1525

作者：

SADLACK, B ^{[1
]}

MERZ, H ^{[1
]}

SCHORLE, H ^{[1
]}

SCHIMPL, A ^{[1
]}

FELLER, AC ^{[1
]}

HORAK, I ^{[1
]}

机构：

[1] MED UNIV LUBECK, INST PATHOL, D-23562 LUBECK, GERMANY

来源：

CELL | 1993年 / 75卷 / 02期

关键词：

D O I：

10.1016/0092-8674(93)80067-O

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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 immunoglobin 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.

引用

页码：253 / 261

页数：9

共 42 条

[41] LYMPHOCYTES ISOLATED FROM THE INTESTINAL LAMINA PROPRIA OF NORMAL NONHUMAN-PRIMATES HAVE INCREASED EXPRESSION OF GENES ASSOCIATED WITH T-CELL ACTIVATION [J].