RGD Reference Report - Quantitative trait loci disposing for both experimental arthritis and encephalomyelitis in the DA rat; impact on severity of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis and antibody isotype pattern. - Rat Genome Database

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Quantitative trait loci disposing for both experimental arthritis and encephalomyelitis in the DA rat; impact on severity of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis and antibody isotype pattern.

Authors: Dahlman, I  Lorentzen, JC  De Graaf, KL  Stefferl, A  Linington, C  Luthman, H  Olsson, T 
Citation: Dahlman I, etal., Eur J Immunol 1998 Jul;28(7):2188-96
RGD ID: 61068
Pubmed: (View Article at PubMed) PMID:9692888
DOI: Full-text: DOI:10.1002/(SICI)1521-4141(199807)28:07<2188::AID-IMMU2188>3.0.CO;2-B

Quantitative trait loci (QTL) controlling inflammatory diseases with different organ specificity may hypothetically either be unique for one disease or shared among different diseases. We have investigated whether five non-MHC QTL controlling susceptibility to experimental arthritis in the DA rat also influence myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in an F2 intercross between inbred DA and PVG.RT1a rats. Two of the five chromosome regions affecting arthritis in the DA rat also regulate phenotypes of EAE. The DA allele at markers in Cia3 (collagen-induced arthritis QTL) on chromosome 4 is associated with more severe EAE and high levels of anti-MOG antibodies of the IgG2c subclass. Since production of antibodies of the IgG2c subclass may be stimulated by Th1 cells, and there is previous evidence that such cells promote EAE, it is possible that both of the studied phenotypes are controlled by the same gene or genes regulating Th1/Th2 cell differentiation. Furthermore, we show that Oia2 (oil-induced arthritis QTL) on chromosome 4 regulates levels of anti-MOG antibodies of the IgG1 subclass and of anti-MOG IgE, but that this gene region does not affect clinical disease severity in our study. Since production of IgE and IgG1 may be stimulated by Th2 cells, this QTL may also control Th1/Th2 bias. We conclude that Cia3 and Oia2 regulate MOG-induced EAE in rats. Furthermore, since both EAE and arthritis phenotypes co-localize to these gene regions, they may harbor genes which are key regulators of pathogenic immune responses.



Phenotype Annotations    

Mammalian Phenotype
Objects Annotated

Strains
DA  (DA)

Objects referenced in this article
Marker D7Arb17 D7Arb17 Rattus norvegicus
Marker D1Arb36 D1Arb36 Rattus norvegicus
Marker D4Arb21 D4Arb21 Rattus norvegicus
Marker D10Mgh1 D10Mgh1 Rattus norvegicus
Marker D4Mgh10 D4Mgh10 Rattus norvegicus
Marker D7Rat44 D7Rat44 Rattus norvegicus
Marker D1Rat212 D1Rat212 Rattus norvegicus
Marker D1Arb37 D1Arb37 Rattus norvegicus
Marker D10Arb22 D10Arb22 Rattus norvegicus
Marker D4Arb24 D4Arb24 Rattus norvegicus
QTL Cia2 Collagen induced arthritis QTL 2 Rattus norvegicus
QTL Cia3 Collagen induced arthritis QTL 3 Rattus norvegicus
QTL Cia4 Collagen induced arthritis QTL 4 Rattus norvegicus
QTL Cia5 Collagen induced arthritis QTL 5 Rattus norvegicus
Strain DA/Bkl null Rattus norvegicus
Strain F344/NHsd F344/NHsd Rattus norvegicus
Gene Gh1 growth hormone 1 Rattus norvegicus
Gene Il2rb interleukin 2 receptor subunit beta Rattus norvegicus
Strain LEW Lewis Rattus norvegicus
QTL Oia2 Oil induced arthritis QTL 2 Rattus norvegicus
QTL Oia3 Oil induced arthritis QTL 3 Rattus norvegicus
Gene Pdgfrb platelet derived growth factor receptor beta Rattus norvegicus
Gene Prkca protein kinase C, alpha Rattus norvegicus
Strain PVG.1AV1 Piebald-Virol-Glaxo Rattus norvegicus
Gene Tgfbr1 transforming growth factor, beta receptor 1 Rattus norvegicus
Gene Timp2 TIMP metallopeptidase inhibitor 2 Rattus norvegicus

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