Content area
Full text
Received Jan 21, 2017; Accepted Jun 4, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Ankylosing spondylitis (AS) is a chronic inflammatory joint disease that chiefly affects the sacroiliac joints and the spine [1]. Radiographs reveal erosive changes at the corners of the vertebral bodies in the early stages of the disease and outgrowth of bony spurs known as syndesmophytes in the later stages [2]. When these syndesmophytes make the adjacent vertebral bodies fuse together, the spine appears as a single piece and is aptly described as a bamboo spine. The pathogenesis of syndesmophyte formation in AS remains unknown.
IL-23 is an immunomodulatory cytokine; the effects of which are mediated by downstream cytokines such as IL-17 and IL-22. Recently, accumulating data suggest that the IL-23/IL-17 axis plays a pivotal role in AS. One of the earliest discoveries that implicated IL-23 signaling in AS was an association with variants in the gene encoding one subunit of the IL-23 receptor (IL-23R) [3], and the association between the IL-23 receptor and AS was confirmed in subsequent studies of individuals of European descent [4] and Chinese population [5]. Subsequently, elevated IL-17 levels were found in the serum and synovial fluid of patients with active AS, undifferentiated spondyloarthropathy (SpA), and psoriatic arthritis (PsA) [6, 7]. Also, increased numbers of IL-23-responsive T cells (including Th17 cells, ROR