Hi SimplySouthern,

The study I referred to is one of the first to try and link variants of ERAP1 to the phenotype or clinical characteristics of AS patients.
Several SNPs of ERAP1 have been identified, namely, rs30187 (which means Lysine is replaced by Arginine at position 528, designated Lys528Arg); rs27044 (Gln730Glu); rs2287987 (Met349Val); rs10050860 (Asp75Asn) and rs17482078 (Arg725Gln). The authors restricted themselves to looking at rs30187 and rs27044 and whether or not these influenced Age of Onset (for a HLA-B27 positive patients) and axial Versus mixed pattern of disease for the early onset sub-group.
Even though those two ERAP1 variants are not contributing to your disease there are the other 3 ERAP1 variants to consider and as you point out the seven or so listed variants within the genetic code of the IL 23 Receptor protein.
IL23 is a very important cytokine (white cell chemical messenger) for AS patients. It is produced predominantly in the gut but unfortuneately there are a type of recently discovered lymphoid cells that are restricted to tendon and ligament attachment sites that are IL23R+ so they will respond to high levels of circulating IL23 by ramping up inflammation at those sites (rather than repairing any tendon micro tears as they are supposed to do).
Since as you have indicated you have six out of seven of the at-risk IL23R SNPs then perhaps for you the IL23/IL23R axis is more of a driver of disease than ERAP1 and may be you might be expected to have considerable issues peripherally and perhaps significant gut issues?

Dx Oct 2006 B27+ undifferentiated spondlyarthropathy (uSpA) with mild sebhorrhoeic dermatitis and mild Inflammatory Bowel Disease (IBD) controlled by NSD since 2007.