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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-05-1383. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-05-1383v1 100/13/4529    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Hall, A. M. Articles by Barker, R. N. Search for Related Content PubMed PubMed Citation Articles by Hall, A. M. Articles by Barker, R. N. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 December 2002, Vol. 100, No. 13, pp. 4529-4536 IMMUNOBIOLOGY Interleukin-10-mediated regulatory T-cell responses to epitopes on a human red blood cell autoantigen Andrew M. Hall, Frank J. Ward, Mark A. Vickers, Lisa-Marie Stott, Stanislaw J. Urbaniak, and Robert N. Barker From the Department of Medicine and Therapeutics, Institute of Medical Sciences, University of Aberdeen Foresterhill, Aberdeen, United Kingdom; and the Academic Transfusion Medicine Unit, Regional Transfusion Centre, Foresterhill, Aberdeen, United Kingdom. Regulatory T cells have been shown to control animal models of immune-mediated pathology by inhibitory cytokine production, but little is known about such cells in human disease. Here we characterize regulatory T-cell responses specific for a human red blood cell autoantigen in patients with warm-type autoimmune hemolytic anemia. Peripheral blood mononuclear cells from patients with autoimmune hemolytic anemia were found either to proliferate and produce interferon- or to secrete the regulatory cytokine interleukin 10 when stimulated in vitro with a major red blood cell autoantigen, the RhD protein. Flow cytometric analysis confirmed that the majority of the responding cells were of the CD4+ phenotype. Serial results from individual patients demonstrated that this bias toward proliferative or interleukin-10 responses was unstable over time and could reverse in subsequent samples. Epitope mapping studies identified peptides from the sequence of the autoantigen that preferentially induced interleukin-10 production, rather than proliferation, and demonstrated that many contain naturally processed epitopes. Responses to such peptides suppressed T-cell proliferation against the RhD protein, an inhibition that was mediated largely by interleukin 10 and dependent on cytotonic T lymphocyte-associated antigen (CTLA-4) costimulation. Antigenic peptides with the ability to stimulate specific regulatory cells may represent a new class of therapeutic agents for immune-mediated disease. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Serafini, M. Andreani, M. Testi, M. Battarra, A. Bontadini, E. Biral, K. Fleischhauer, S. Marktel, G. Lucarelli, M. G. Roncarolo, et al. Type 1 regulatory T cells are associated with persistent split erythroid/lymphoid chimerism after allogeneic hematopoietic stem cell transplantation for thalassemia Haematologica, October 1, 2009; 94(10): 1415 - 1426. [Abstract] [Full Text] [PDF] A. D'Ambrosio, M. Colucci, O. Pugliese, F. 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