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Titolo:
GENETIC-CONTROL OF SUSCEPTIBILITY TO COLLAGEN-INDUCED ARTHRITIS IN T-CELL RECEPTOR BETA-CHAIN TRANSGENIC MICE
Autore:
MORI L; DELIBERO G;
Indirizzi:
UNIV BASEL HOSP,DEPT RES,HEBELSTR 20 CH-4031 BASEL SWITZERLAND
Titolo Testata:
Arthritis and rheumatism
fascicolo: 2, volume: 41, anno: 1998,
pagine: 256 - 262
SICI:
0004-3591(1998)41:2<256:GOSTCA>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
II COLLAGEN; RHEUMATOID-ARTHRITIS; CENTROMERIC REGION; COMPLEMENT C5; MOUSE STRAIN; AUTOIMMUNITY; INDUCTION; GLYCOSYLATION; LOCALIZATION; ANTIBODIES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
L. Mori e G. Delibero, "GENETIC-CONTROL OF SUSCEPTIBILITY TO COLLAGEN-INDUCED ARTHRITIS IN T-CELL RECEPTOR BETA-CHAIN TRANSGENIC MICE", Arthritis and rheumatism, 41(2), 1998, pp. 256-262

Abstract

Objective. To study the genes in the mouse background which predispose to the development of collagen-induced arthritis (CIA). Methods. T cell receptor beta transgenic (TCR beta L) mice that have a T cell repertoire that predisposes to the development of CU were used. Classic genetic studies and microsatellite gene mapping were done in (SWR-beta Lx DBA/1)F-2 hybrid mice. Results. Besides TCR beta, major histocompatibility complex class II, and Igh-C, at least 2 other genes are absolutely required for CU development in these mice. A strict association of CU with the presence of functional complement C5 allele (Hc(1)) was found, suggesting that Hc(1) or a closely linked gene might be one of these essential genes. Conclusion. This study provides new evidence ofthe pathogenetic role of complement C5 in CIA. Furthermore, these transgenic mice may facilitate molecular identification of other genes that predispose to CIA.

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Documento generato il 27/11/20 alle ore 04:28:46