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Titolo:
ULCERATIVE COLITIS-LIKE DISEASE IN MICE WITH A DISRUPTED INTERLEUKIN-2 GENE
Autore:
SADLACK B; MERZ H; SCHORLE H; SCHIMPL A; FELLER AC; HORAK I;
Indirizzi:
UNIV WURZBURG,INST VIROL & IMMUNOBIOL,VERSBACHER STR 7 D-97078 WURZBURG GERMANY MED UNIV LUBECK,INST PATHOL D-23562 LUBECK GERMANY
Titolo Testata:
Cell
fascicolo: 2, volume: 75, anno: 1993,
pagine: 253 - 261
SICI:
0092-8674(1993)75:2<253:UCDIMW>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFLAMMATORY BOWEL-DISEASE; EMBRYONIC STEM-CELLS; GERM-LINE TRANSMISSION; T-CELLS; INTRAEPITHELIAL LYMPHOCYTES; RECOMBINANT INTERLEUKIN-2; PERIPHERAL-BLOOD; GUT EPITHELIUM; HPRT GENE; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
B. Sadlack et al., "ULCERATIVE COLITIS-LIKE DISEASE IN MICE WITH A DISRUPTED INTERLEUKIN-2 GENE", Cell, 75(2), 1993, pp. 253-261

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 highnumber 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.

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Documento generato il 28/11/20 alle ore 15:35:27