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10.1002/art.38763

http://scihub22266oqcxt.onion/10.1002/art.38763
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C4198528!4198528!24980965
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suck abstract from ncbi


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pmid24980965      Arthritis+Rheumatol 2014 ; 66 (10): 2793-803
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  • Role of PPM1A and anti-PPM1A Autoantibodies in Ankylosing Spondylitis #MMPMID24980965
  • Kim YG; Sohn DH; Zhao X; Sokolove J; Lindstrom TM; Yoo B; Lee CK; Reveille JD; Taurog JD; Robinson WH
  • Arthritis Rheumatol 2014[Oct]; 66 (10): 2793-803 PMID24980965show ga
  • Objective: Although ankylosing spondylitis (AS) is driven by immunemediated processes, little is known about the presence and role of autoantibodies in this disease. Methods: We performed human protein microarray analysis of sera derived from patients with AS and other autoimmune disorders to identify autoantibodies associated specifically with AS, and identified autoantibody targeting of protein phosphatase magnesium-dependent 1A (PPM1A) in AS. We performed ELISA analysis of sera from two independent AS cohorts to confirm autoantibody targeting of PPM1A, and to assess associations between levels of anti-PPM1A antibodies and AS disease severity or response (as measured by BASDAI score) to anti-TNF therapy. Levels of anti-PPM1A antibodies were also evaluated in sera from transgenic rats overexpressing HLA-B27 and human ?2-microglobulin. The expression of PPM1A was assessed by immunohistochemistry in synovial tissues from patients with AS, rheumatoid arthritis, or osteoarthritis. The role of PPM1A on osteoblast differentiation was investigated by gene knock-down and overexpression. Results: AS was associated with autoantibody targeting of PPM1A, and levels of anti-PPM1A autoantibodies were significantly higher in patients with more advanced sacroiliitis and correlated with BASDAI score after treatment with anti-TNF agents. The levels of anti-PPM1A autoantibodies were also higher in sera of transgenic rats that are prone to develop AS than in those that are not. PPM1A was expressed in AS synovial tissue, and PPM1A overexpression promoted osteoblast differentiation, whereas PPM1A knockdown suppressed it. Conclusions: Anti-PPM1A autoantibodies are present in AS, and our findings suggest that PPM1A may contribute to the pathogenic bone ankylosis characteristic of AS.
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