![]() ![]() ![]() Positional cloning of PIA7 and PIA4 have identified Clec4b and Ncf1 as the regulating genes for arthritis severity and onset as well as controlling innate and adaptive immune responses. PIA4 and PIA7 QTLs, on chromosome 12 and chromosome 4 respectively, are the strongest regulators of multiple arthritis models in rats. Linkage studies performed by our lab and others in F2 crosses between a resistant inbred strain (i.e., E3 or PVG) and a susceptible counterpart (i.e., DA) identified the major quantitative trait loci (QTL) that regulate clinical score, onset and paw swelling in PIA. A single intradermal injection at the tail base of pure adjuvants such as pristane is enough to induce a severe arthritis-like phenotype (pristane-induced arthritis, PIA) in many rat strains. Animal models of complex diseases, such as arthritis, offer a possibility not only to position the underlying polymorphism but also to study their pathogenic role in a controlled setting. However, these variants explain only a limited degree of the estimated heritability and very few, if any, of the underlying genes have been identified and their functional role elucidated. Genome-wide association studies identified several major histocompatibility complex (MHC) and non-MHC loci associated with RA. RA is a complex disease due to the intricate interplay between genetic and environmental factors. Rheumatoid arthritis (RA) is an autoimmune disease that affects 0.5 to 1% of the population and if untreated often leads to irreversible joint damage.
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