{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,28]],"date-time":"2025-11-28T17:18:44Z","timestamp":1764350324395},"reference-count":46,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T00:00:00Z","timestamp":1475539200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T00:00:00Z","timestamp":1475539200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Sci Rep"],"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ankylosing spondylitis (AS) is a chronic axial spondyloarthritis (SpA) resulting in back pain and progressive spinal ankyloses. Currently, there are no effective therapeutics targeting AS largely due to elusive pathogenesis mechanisms, even as potential candidates such as HLA-B27 autoantigen have been identified. Herein, we employed a proteoglycan (PG)-induced AS mouse model together with clinical specimens, and found that the complement system was substantially activated in the spinal bone marrow, accompanied by a remarkable proportion alteration of neutrophils and macrophage in bone marrow and spleen, and by the significant increase of TGF-\u03b21 in serum. The combined treatment with a bacteria-derived complement inhibitor Efb-C (<jats:underline>C<\/jats:underline>-terminal of<jats:underline>e<\/jats:underline>xtracellular<jats:underline>f<\/jats:underline>ibrinogen-<jats:underline>b<\/jats:underline>inding protein of<jats:italic>Staphylococcus aureus<\/jats:italic>) remarkably retarded the progression of mouse AS by reducing osteoblast differentiation. Furthermore, we demonstrated that two important modulators involved in AS disease, TGF-\u03b21 and RANKL, were elevated upon<jats:italic>in vitro<\/jats:italic>complement attack in osteoblast and\/or osteoclast cells. These findings further unravel that complement activation is closely related with the pathogenesis of AS, and suggest that complement inhibition may hold great potential for AS therapy.<\/jats:p>","DOI":"10.1038\/srep34643","type":"journal-article","created":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T11:50:23Z","timestamp":1475581823000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Inhibition of Complement Retards Ankylosing Spondylitis Progression"],"prefix":"10.1038","volume":"6","author":[{"given":"Chaoqun","family":"Yang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peipei","family":"Ding","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qingkai","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Long","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianquan","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Enjie","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Na","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianfeng","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guang","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weiguo","family":"Hu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuhui","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2016,10,4]]},"reference":[{"key":"BFsrep34643_CR1","doi-asserted-by":"crossref","first-page":"416","DOI":"10.1007\/s11926-011-0202-x","volume":"13","author":"M Ronneberger","year":"2011","unstructured":"Ronneberger, M. & Schett, G. Pathophysiology of spondyloarthritis. Curr Rheumatol Rep. 13, 416\u2013420 (2011).","journal-title":"Curr Rheumatol Rep."},{"key":"BFsrep34643_CR2","doi-asserted-by":"crossref","first-page":"E2","DOI":"10.3171\/FOC\/2008\/24\/1\/E2","volume":"24","author":"E Dakwar","year":"2008","unstructured":"Dakwar, E., Reddy, J., Vale, F. L. & Uribe, J. S. A review of the pathogenesis of ankylosing spondylitis. Neurosurg Focus 24, E2 (2008).","journal-title":"Neurosurg Focus"},{"key":"BFsrep34643_CR3","doi-asserted-by":"crossref","first-page":"55","DOI":"10.2174\/157339706775697044","volume":"2","author":"A Ebringer","year":"2006","unstructured":"Ebringer, A., Rashid, T., Wilson, C., Ptaszynska, T. & Fielder, M. Ankylosing Spondylitis, HLA-B27 and Klebsiella - An Overview: Proposal for Early Diagnosis and Treatment. 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