One theme in our group is to understand how specific HLA-B*27 subtypes pre-dispose to inflammatory autoimmune condition, most notably Ankylosing Spondylitis (AS), a condition that affects the spine and specific joints. This association has been recognised for over 5 decades, but the biological basis of disease initiation is not well understood. Through international collaboration, we recently re-explored an original disease model suggesting that a case of mistaken identity (autoimmunity) contributes to disease pathology where CD8+ T cells initially triggered by microbial epitopes bound to HLA-B*27 subsequently attack HLA-B*27-bound to self-peptides.