Abstract
Ankylosing Spondylitis (AS) is a chronic inflammatory disease that characterized by enthesitis and subsequent syndesmophytes in spinal joints and peripheral joints. However, the exact pathogenesis of AS is still unknown. Recent studies indicate that serum concentrations of interleukin-23 (IL-23) are elevated in AS and the expression of IL-23 in vivo is sufficient to phenocopy the human disease such as spondyloarthropathy (SpA), with the specific and characteristic development of enthesitis and entheseal new bone formation in the initial complete absence of synovitis. But it remains unclear what might be the cause that is related to the elevation of IL-23 in enthesis. Macrophage, which is a primary source of IL-23 in response to inflammatory stimulation, has been detected around the abnormal vascular structure at enthesis in SpA. Besides, the plasticity and polarization of macrophage plays a vital role in local inflammation and immune response. Here, we proposed a hypothesis that macrophages residing in and migrating through the abnormal vascular structure to enthesis in the inflammatory state are an essential source of IL-2, which alone can induce enthesitis and promote abnormal new bone formation in AS.
Highlights
Ankylosing spondylitis is a common inflammatory disease which often affects the function of axial joints and peripheral joints
We propose that macrophage residing in enthesis and migrating through the abnormal vascular structure to enthesis from distance would be an important source of IL-2, which would drive enthesitis in vivo
Enthesitis is a distinct characterization of spondyloarthropathy and the cells that are involved in inflammatory enthesis are the key to reveal SpA
Summary
Ankylosing spondylitis is a common inflammatory disease which often affects the function of axial joints and peripheral joints. Mechanical stress injury may explain the clinical differences of inflammatory changes of entheses but why it is prone to occur especially in the SpA? These results suggest that pro-inflammatory M1 macrophage is the likely a main contributor to local tissue injury to immune disease such as spondyloarthropathy. Macrophages, which arise in spondyloarthropathies peripheral blood and early inflammatory lesions [16], have been proved to be associated with the HLA-B27 gene.
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