Macrophage in Enthesis: A Likely Contributing Factor to Enthesitis through IL-23 in Ankylosing SpondylitisQin Yang1, Da He Li2, Bin Chen2, Jia Li2 and Wei-dong Xu2*
- *Corresponding Author:
- Weidong Xu
Department of Orthopedics, Changhai Hospital
The Second Military Medical University
20043, Shanghai, P. R. China
Tel: +86 021 8187 3393
E-mail: [email protected]
Received Date: November 27, 2014; Accepted Date: December 18, 2014; Published Date: December 29, 2014
Citation: Yang Q, Li DH, Chen B, Li J, Xu W (2014) Macrophage in Enthesis: A Likely Contributing Factor to Enthesitis through IL-23 in Ankylosing Spondylitis. Rheumatology (Sunnyvale) S4:006. doi: 10.4172/2161-1149.S4-006
Copyright: © 2014 Yang Q, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.