Ankylosing spondylitis (AS) is a chronic systemic inflammatory rheumatic disorder of uncertain aetiology that primarily affects the axial skeleton (sacroiliac joints and spine). Although the pathogenesis of the disease is poorly understood, immune-mediated mechanisms involving human leukocyte antigen (HLA)-B27, inflammatory cellular infiltrates, cytokines, such as tumor necrosis factor (TNF)-a and interleukin-10 (IL-10), as well as genetic and environmental factors, are thought to have key roles [1]. Based on the strong association between HLA-B27 and the disease, Uchanska-Ziegler and Ziegler recently proposed that AS could be ab 2-microglobulin (b2m)-deposition disease, with parallels to b2m-amyloidosis observed in long-term dialysis patients [2]. The essence of their hypothesis is that cells bearing AS-associated HLA-B27 subtypes might exhibit a higher rate of b2m-dissociation from surface-expressed HLA-B27 molecules; b2m molecules might accumulate and become trapped in synovia where they bind to collagen, form amyloid deposits or interact with synovial fibroblasts in which they induce the synthesis and secretion of proteins involved in tissue destruction. Some of the deposited b2m