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Blood, 12 March 2009, Vol. 113, No. 11, pp. 2568-2577. Prepublished online as a Blood First Edition Paper on December 3, 2008; DOI 10.1182/blood-2008-03-148288. This Article Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2008-03-148288v1 113/11/2568    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Zhang, X.-L. Articles by Hou, M. Search for Related Content PubMed PubMed Citation Articles by Zhang, X.-L. Articles by Hou, M. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 31, 2008 Accepted November 24, 2008 De novo induction of platelet-specific CD4+CD25+ regulatory T cells from CD4+CD25- cells in patients with idiopathic thrombocytopenic purpura Xiao-Lin Zhang, Jun Peng*, Jian-Zhi Sun, Jia-Jun Liu, Cheng-Shan Guo, Zhen-Guang Wang, Yuan Yu, Yan Shi, Ping Qin, Shu-Guang Li, Li-Ning Zhang, and Ming Hou Department of Hematology, Qilu Hospital, Shandong University, Jinan, China The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Jinan, China Department of Hematology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China Department of Hematology, Second Hospital, Shandong University, Jinan, China Department of Science and Technology, Shandong University, Jinan, China Institute of Immunology, School of Medicine, Shandong University, Jinan, China * Corresponding author; email: junpeng88{at}sina.com.cn. CD4+CD25+ regulatory T cells (Treg) play the critical role in maintenance of peripheral immune tolerance. However, the numbers of naturally occurring Treg (nTreg) that can be isolated from periphery are far too small to be clinically effective. The isolation and expansion of nTreg for treatment of autoimmune diseases encounters great difficulties. Whether autoantigen-specific Treg could be converted from CD4+CD25- T cells in patients with autoimmune diseases has not been reported. Here, we demonstrated that platelet glycoprotein (GP)-specific induced Treg (GP-iTreg) could be generated de novo from non-regulatory CD4+CD25-CD45RA+ cells in patients with idiopathic thrombocytopenic purpura (ITP), and induced both antigen-specific and linked suppression. GP-iTreg mediated regulatory effects via modulating the T-cell-stimulatory capacity of DCs. By investigating the gene expression profile of iTreg-modulated DCs, we provided a genome-wide assessment of the changes induced by antigen-specific iTreg and identified that the Toll-like receptor, Notch and TGF-beta signaling pathways were related to the GP-specific tolerance, with the Toll-like receptor pathway being dominant. The findings in patients with ITP will facilitate our understanding of the mechanisms of induction and maintenance of autoantigen-specific tolerance and highlight the considerable potential of antigen-specific iTreg for targeted immunotherapy in human autoimmune diseases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Platelet antigen-induced regulation in ITP John W. Semple Blood 2009 113: 2373. [Full Text] [PDF] This article has been cited by other articles: J. W. Semple Platelet antigen-induced regulation in ITP Blood, March 12, 2009; 113(11): 2373 - 2373. [Full Text] [PDF]

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