Research Papers: Pathology:
Circulation autoantibody against Lamin A/C in patients with Sjögren’s syndrome
Metrics: PDF 1751 views | HTML 2883 views | ?
Abstract
Wen Zhang1,*, Chunyan Zhang2,*, Peng Chen1, Chunhe Yang1, Xianfeng Gan1, Muhammad Hussain1, Yiping Xun1, Yaping Tian2 and Hongwu Du1
1 112 Lab, School of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, China
2 Department of Clinical Biochemistry, Chinese PLA General Hospital, Beijing, China
* These authors have contributed equally to this work
Correspondence to:
Hongwu Du, email:
Yaping Tian, email:
Keywords: autoimmune diseases; Sjögren’s syndrome; Lamin A/C; autoantigen; similar antigen epitopes; Pathology Section
Received: April 15, 2016 Accepted: October 25, 2016 Published: November 09, 2016
Abstract
Lamin A/C proteins are major components of nuclear laminae and were encoded by the LMNA gene. Recent studies have found that in addition to provides nuclear-membrane strength; it also regulates the gene expression. Lamin A/C has been confirmed as an autoantigen in RA, SLE and vasculitis. Anti-Lamin A/C antibodies also have been found by indirect immunofluorescence method. In this study, we used various research methods to confirm Lamin A/C is an autoantigen in Han Chinese patients with confirmed Sjögren’s syndrome (SS). To further investigate the relationship between the autoimmune disease antigens, we compared the amino acid sequence of Lamin A/C epitope and several common antigens’ antigenic determinant. As a result, we found that Lamin A/C has similar epitopes with U1RNP. It means that the potential relationship exist between Lamin A/C and U1RNP. Clinical data we collected also showed that anti-Lamin A/C and anti-U1RNP antibodies always appear in same serum sample. Therefore, we speculated that cross-reaction may take place between antigen and potential antigen, which have similar epitope. Then, by epitope spreading, the potential antigen can be a new autoantigen. Our study provided a new thinking for further research about the relationship between autoantigens and their development mechanism in autoimmune diseases.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 13256