This review is concerned with a number of recent publications that contribute to current thinking on the pathogenesis of spondyloarthritis. The areas covered include the lymphocyte population in the enthesis, which is thought to drive enthesitis, and hence clinical manifestations. The debate on how HLA-B27 is implicated in inflammation is also considered, together with recent and contradictory evidence on the effects of the peptide-trimming enzyme ERAP1 on B27 expression and hence susceptibility to spondylitis. Lastly, a recent report on the role of the gut microbiome in an important model of spondyloarthritis is considered.