Genetically determined high activities of the TNF-alpha, IL23/IL17, and NFkB pathways were associated with increased risk of ankylosing spondylitis.

Jacob SodeSteffen BankUlla VogelPaal Skytt AndersenSigne Bek SørensenAnders Bo BojesenMalene Rohr AndersenIvan BrandslundRam Benny DessauHans Jürgen HoffmannBente GlintborgMerete Lund HetlandHenning LochtNiels Henrik HeegaardVibeke Andersen

Published in: BMC medical genetics (2018)

We replicated associations between AS and the polymorphisms in TNF (rs1800629), TNFRSF1A (rs4149570), and IL23R (rs11209026). Furthermore, we identified novel risk loci in TNF (rs361525), IL18 (rs187238), TLR1 (rs4833095), TLR4 (rs1554973), and LY96 (rs11465996) that need validation in independent cohorts. The results suggest that genetically determined high activity of the TNF-α, IL23/IL17, and NFkB pathways increase risk of AS.

Keyphrases

rheumatoid arthritis
ankylosing spondylitis
inflammatory response
immune response
disease activity
systemic lupus erythematosus
dna methylation