Thanks jroc and Simply Southern, you inspired me to pay the $280 (Australian, including post) to get tested by 23andme.

Basically my results are identical to Simply Southern, that is, I knew already that I was HLA-B27+, and the genetic test showed that I carried no ‘at risk’ ERAP1 alleles, but carried 6 out of 8 IL23R variants with bad repute.

According to me (and no one else), and according to the ‘ubiquitous pathogen exposure hypothesis’, HLA-B27+ individuals who also carry ‘at risk’ alleles of ERAP1, will develop a spondyloarthropathy when activated gut dendritic cells stimulate gut-mucosal memory T cells to be polarised toward a Th17 phenotype. Elevated levels of circulating IL23 will drive the disease processes such that those individuals who also carry ‘at risk’ alleles of IL23R will also suffer significant peripheral enthesitis and IBD / Crohns-like symptoms on top of the axial aspects of AS.

Individuals who are B27+ and have ‘at risk’ ERAP1 drivers, but not IL23R risk alleles might be expected to present as classic early onset AS but without significant gut or peripheral symptoms? Such cases might feel they are unaffected by diet?

In the case of someone like me, with B27 and IL23 drivers, but without ‘risk’ ERAP1 alleles, they might be expected to suffer gut and peripheral symptoms with lesser axial symptoms (no fusion).

I’d encourage more KickAS’ers to get tested.
Regards David.

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