The pathogenetic role of HLA-B27 in the spon-dylarthritides (SpA) is an elusive problem that remains unsolved 37 years after the discovery of the extraordinary association of this antigen with ankylosing spondylitis (AS) (1,2) and almost 20 years after the establishment of a transgenic animal model (3) in which the direct involvement of B27 in the pathogenesis of these diseases was demonstrated. In the absence of definitive evidence for the mechanism of this association, 3 major hypotheses are currently the focus of intense debate. First is the arthritogenic peptide hypothesis (4), which is based on the canonical antigen-presenting properties of B27.
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