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Clinical and Developmental Immunology
Volume 2013, Article ID 206298, 5 pages
Research Article

A Possible Role of HMGB1 in DNA Demethylation in CD4+ T Cells from Patients with Systemic Lupus Erythematosus

1Department of Dermatology and Epigenetic Research Center, Key Laboratory of Diabetes Immunology of Ministry of Education, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
2Department of Oncology, Third Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
3Department of Medicine, The University of Hong Kong, Hong Kong

Received 25 March 2013; Revised 2 August 2013; Accepted 2 August 2013

Academic Editor: Guixiu Shi

Copyright © 2013 Yaping Li et al. 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.


The aberrant activity of CD4+ T cells in patients with systemic lupus erythematosus (SLE) is associated with DNA hypomethylation of the regulatory regions in CD11a and CD70 genes. Our previous studies demonstrated that Gadd45a contributes to the development of SLE by promoting DNA demethylation in CD4+ T cells. In this study, we identified proteins that bind to Gadd45a in CD4+ T cells during SLE flare by using the method of co-immunoprecipitation and mass spectrometry, High mobility group box protein 1 (HMGB1) is one of identified proteins. Furthermore, gene and protein expression of HMGB1 was significantly increased in SLE CD4+ T cells compared to controls, and HMGB1 mRNA was correlated with CD11a and CD70 mRNA. A significant, positive correlation was found between HMGB1 mRNA and SLEDAI for SLE patients. Our data demonstrate that HMGB1 binds to Gadd45a and may be involved in DNA demethylation in CD4+ T cells during lupus flare.