Immunopathogenesis of Ankylosing Spondylitis: An Updated Review

Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory arthritis of unknown etiology, which belongs to a group of conditions known as spondyloarthropathies that comprises psoriatic arthritis, reactive arthritis, and enteropathic arthritis. AS causes pathologic new-bone formation in the axial skeleton, and leads to chronic pain, axial fusion, deformity, disability and skeletal fracture. Several genetic and environmental factors are known to be associated with AS. Notwithstanding the fact that a multitude of genes, such as human leukocyte antigen B27 (HLA-B27), endoplasmic reticulum-associated aminopeptidase 1 (ERAP1), and interleukin-23 receptor (IL-23R) have been previously speculated to be associated with individuals’ susceptibility to AS, no consensus about their precise role in the etiopathogenesis of AS has been reached. In the present study, we summarize the current literature on the immunogenetics of AS and contemporize the research advancement that has been made over the past decade.