Abstract
Ankylosing spondylitis (AS) is a chronic disease characterized by inflammatory back pain and progressive stiffening of the spine. The association between AS and HLA-B27, a major histocompatibility complex class I molecule, has been known since 1973. Despite intense interest and active investigations into the role of HLA-B27 in the pathogenesis of AS, the specific role of HLA-B27 in AS is not yet known. One of the postulated hypotheses states that misfolding of the HLA-B27 heavy chains causes activation of the unfolded protein response, which sensitizes cells to proinflammatory cytokine production. The IL-23/Th17 axis may play an important role in this pathway. As AS is a multifactorial disease, not only genetic factors are of interest, but environmental factors, such as biomechanical stress, may also play an important role in the pathogenesis. None of the postulated mechanisms regarding the pathogenesis of AS have been strictly proven, but current results from studies are promising.
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