Solving the pathogenesis of ankylosing spondylitis

- HLA-B associations of AS are complex, with protective and risk associations in addition to the associations with HLA-B27 having been established.
- Interaction between ERAP1 and HLA-B27 and -B40 has been demonstrated, indicating that ERAP1 works probably by similar mechanisms, with these genes to cause AS.
- AS appears to be driven by interaction between the gut microbiome and host immune system offering the potential to treat the condition by gut targeted therapies.
- HLA-B27 forms homodimers, and there is strong evidence that these operate in AS to induce AS through interactions with KIR bearing immune cells.