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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4528-4538. Prepublished online as a Blood First Edition Paper on February 1, 2007; DOI 10.1182/blood-2006-09-044388. This Article Full Text (PDF) All Versions of this Article: blood-2006-09-044388v1 109/10/4528    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 Sukati, H. Articles by Barker, R. N Search for Related Content PubMed PubMed Citation Articles by Sukati, H. Articles by Barker, R. N Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 5, 2006 Accepted December 15, 2006 Mapping helper T cell epitopes on platelet membrane glycoprotein IIIa in chronic autoimmune thrombocytopenic purpura Hosea Sukati, Henry G Watson, Stanislaw J Urbaniak, and Robert N Barker* Dept of Medicine and Therapeutics, University of Aberdeen, United Kingdom Department of Haematology, Aberdeen Royal Infirmary, United Kingdom Academic Transfusion Medicine Unit, Regional Transfusion Centre, Aberdeen, United Kingdom * Corresponding author; email: r.n.barker{at}abdn.ac.uk. Chronic autoimmune thrombocytopenic purpura (AITP) is associated with autoantibodies specific for platelet membrane components, often including glycoprotein GPIIIa. T helper (Th) cells reactive with GPIIIa, which are capable of driving the autoantibody response, are activated in AITP, and the aim here was to map the epitopes that they recognize. Peripheral blood mononuclear cells (PBMC) were obtained from 31 patients with AITP and 30 control donors, and stimulated with a panel of 86 overlapping synthetic 15-mer peptides spanning the complete sequence of GPIIIa. One or more peptides elicited recall proliferation by PBMC from 28 of the patients, and, typically, multiple sequences were stimulatory. In contrast, responses in healthy control donors were rare (2=115.967; p=<0.001). It was confirmed that the proliferating PBMC from patients were cells of the CD3+CD4+ helper phenotype that were MHC class II restricted. Despite variation between different cases of AITP, particular sequences were commonly recognized, with PBMC from 24 patients (77%) responding to one or more of the four most dominant peptides. Mapping such dominant autoreactive helper epitopes is the first step in the development of new approaches to the treatment of AITP, based on the use of peptides to tolerize Th cells specific for platelet glycoproteins. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. B. Cines, J. B. Bussel, H. A. Liebman, and E. T. Luning Prak The ITP syndrome: pathogenic and clinical diversity Blood, June 25, 2009; 113(26): 6511 - 6521. [Abstract] [Full Text] [PDF] X.-L. Zhang, J. Peng, J.-Z. Sun, J.-J. Liu, C.-S. Guo, Z.-G. Wang, Y. Yu, Y. Shi, P. Qin, S.-G. Li, et al. De novo induction of platelet-specific CD4+CD25+ regulatory T cells from CD4+CD25- cells in patients with idiopathic thrombocytopenic purpura Blood, March 12, 2009; 113(11): 2568 - 2577. [Abstract] [Full Text] [PDF] B. Olsson, B. Ridell, L. Carlsson, S. Jacobsson, and H. Wadenvik Recruitment of T cells into bone marrow of ITP patients possibly due to elevated expression of VLA-4 and CX3CR1 Blood, August 15, 2008; 112(4): 1078 - 1084. [Abstract] [Full Text] [PDF]

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