1. J Immunol. 1998 Oct 15;161(8):4411-9.
Localization of quantitative trait loci regulating adjuvant-induced arthritis in
rats: evidence for genetic factors common to multiple autoimmune diseases.
Kawahito Y(1), Cannon GW, Gulko PS, Remmers EF, Longman RE, Reese VR, Wang J,
Griffiths MM, Wilder RL.
Author information:
(1)The Inflammatory Joint Diseases Section, Arthritis and Rheumatism Branch,
National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda,
MD 20892-1820, USA.
Adjuvant-induced arthritis (AIA) in rats is a widely used autoimmune experimental
model with many features similar to rheumatoid arthritis (RA). To identify
potential genetic regulatory mechanisms in RA, we conducted genome-wide linkage
analysis in F2 progeny of arthritis-susceptible Dark Agouti (DA) and relatively
resistant Fischer 344 (F344) inbred rats. We compared the data with our
previously reported investigation of collagen-induced arthritis (CIA), which was
expanded in the follow-up study reported in this work. We found two quantitative
trait loci (QTLs) in common, i.e., Aia1/Cia1 on chromosome 20, which includes the
MHC, and Aia3/Cia3 on chromosome 4. We also identified a second unique QTL in
AIA, Aia2, on chromosome 4. Interestingly, the QTL region on chromosome 4
(Aia3/Cia3), like the MHC, appears to be involved in several other autoimmune
diseases in rats, including insulin-dependent diabetes, thyroiditis, and
experimental autoimmune uveitis. Moreover, an analysis of conserved synteny among
rats, mice, and humans suggested that Aia2 and Aia3/Cia3, like Aia1/Cia1, contain
candidate genes for several autoimmune/inflammatory diseases in mice and humans,
including diabetes, systemic lupus erythematosus, inflammatory bowel disease,
asthma/atopy, multiple sclerosis, and RA. The rat models appear to provide a
powerful complementary approach to identify and characterize candidate genes that
may contribute to autoimmune diseases in several species.
PMID: 9780220 [PubMed - indexed for MEDLINE]
PUBMED: 9780220
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