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Titolo:
Identification of four new quantitative trait loci regulating arthritis severity and one new quantitative trait locus regulating autoantibody production in rats with collagen-induced arthritis
Autore:
Griffiths, MM; Wang, JP; Joe, B; Dracheva, S; Kawahito, Y; Shepard, JS; Reese, VA; McCall-Vining, S; Hashiramoto, A; Cannon, GW; Remmers, EF; Wilder, RL;
Indirizzi:
Univ Utah, Hlth Sci Ctr, Sch Med, Dept Med,Div Rheumatol, Salt Lake City, UT 84132 USA Univ Utah Salt Lake City UT USA 84132 matol, Salt Lake City, UT 84132 USA Dept Vet Affairs Med Ctr, Salt Lake City, UT USA Dept Vet Affairs Med CtrSalt Lake City UT USA r, Salt Lake City, UT USA NIAMSD, NIH, Bethesda, MD 20892 USA NIAMSD Bethesda MD USA 20892NIAMSD, NIH, Bethesda, MD 20892 USA
Titolo Testata:
ARTHRITIS AND RHEUMATISM
fascicolo: 6, volume: 43, anno: 2000,
pagine: 1278 - 1289
SICI:
0004-3591(200006)43:6<1278:IOFNQT>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; GENOME-WIDE LINKAGE; RHEUMATOID-ARTHRITIS; SUSCEPTIBILITY LOCI; GENETIC DISSECTION; DISEASE SEVERITY; IMMUNE-RESPONSE; GK RAT; BB RAT; COMPLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Griffiths, MM Univ Utah, Hlth Sci Ctr, Sch Med, Dept Med,Div Rheumatol, Room 4B200,50 N Med Dr, Salt Lake City, UT 84132 USA Univ Utah Room 4B200,50 N Med Dr Salt Lake City UT USA 84132
Citazione:
M.M. Griffiths et al., "Identification of four new quantitative trait loci regulating arthritis severity and one new quantitative trait locus regulating autoantibody production in rats with collagen-induced arthritis", ARTH RHEUM, 43(6), 2000, pp. 1278-1289

Abstract

Objective. Collagen-induced arthritis (CIA) is a polygenic model of experimentally induced autoimmunity and chronic joint inflammation. This study maps genetic loci that regulate CW susceptibility in DA/Bkl (Dt) and BN/SsNHsd (BN) rats. Methods. Genome scans covering chromosomes 1-20 and internal mapping techniques using 159 simple sequence-length polymorphism markers were used to identify quantitative trait loci (QTLs) that regulate CIA in (DA x BN)F-2 hybrids. Serum antibody titers to type II collagen were determined by enzyme-linked immunosorbent assay. Results. DA rats were high responders to porcine type II collagen (PII) and developed severe CIA (100%). BN rats were low responders to PII and resistant to CIA (0%). BN genes strongly repressed PII-induced CIA. Only 12% of (DA x BN)F-I rats (7 of 60) and 31% of (DA x BN)F-2 rats (307 of 1,004) developed CIA. Three new QTLs (Cia11, Cia12, and Cia13) with significant logarithm of odds (LOD) scores of 5.6, 4.6, and 4.5, respectively plus a suggestive QTL (Cia14*, LOD 3.0) regulating arthritis severity were identified on chromosomes,7, 12, 1, and 19, A new QTL, Ciaa3, associating with anticollagen antibody titer (antibody to PII LOD 6.5; antibody to rat type Il collagen LOD 5.2) mapped to chromosome 9. Of 10 CIA QTLs previously identified in (DA x F344) and (DA x ACI) rats, only Cia1 in the major histocompatibility complex and a region coincident to Cia5 on chromosome 10 (LOD >8.0) influenced CIA severity in (DA x BN)F-2 rats. Conclusion. Since CIA. exhibits many of the pathologic features of rheumatoid arthritis, the data indicate that the variety of genetic elements regulating human autoimmune and rheumatic diseases may be much larger and more varied than originally envisioned.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 08:56:10