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Blood, 15 December 2007, Vol. 110, No. 13, pp. 4312-4318. Prepublished online as a Blood First Edition Paper on August 28, 2007; DOI 10.1182/blood-2007-07-100008. This Article Full Text (PDF) All Versions of this Article: blood-2007-07-100008v1 110/13/4312    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 Yamaguchi, Y. Articles by Kuwana, M. Search for Related Content PubMed PubMed Citation Articles by Yamaguchi, Y. Articles by Kuwana, M. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 9, 2007 Accepted August 23, 2007 Excessive exposure to anionic surfaces maintains autoantibody response to 2-Glycoprotein I in patients with antiphospholipid syndrome Yukie Yamaguchi, Noriyuki Seta, Junichi Kaburaki, Kazuko Kobayashi, Eiji Matsuura, and Masataka Kuwana* Department of Environmental immuno-dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan Department of Internal Medicine, Tokyo Electric Power Company Hospital, Tokyo, Japan Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmacuetical Sciences, Okayama, Japan * Corresponding author; email: kuwanam{at}sc.itc.keio.ac.jp. Antiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder associated with autoantibodies to phospholipid (PL)-binding proteins, such as 2-glycoprotein I (2GPI). We have recently reported that binding of 2GPI to anionic PL facilitates processing and presentation of the cryptic 2GPI epitope that activates pathogenic autoreactive T cells. To clarify mechanisms that induce sustained presentation of the dominant antigenic 2GPI determinant in APS patients, T cell proliferation induced by 2GPI-treated phosphatidylserine liposome (2GPI/PS) was evaluated in bulk peripheral blood mononuclear cell cultures. T cells from APS patients responded to 2GPI/PS in the presence of IgG anti-2GPI antibodies derived from APS plasma, and this response was completely inhibited either by the depletion of monocytes or by the addition of anti-FcRI antibody. These findings indicate that efficient presentation of the cryptic determinants can be achieved by monocytes undergoing FcRI-mediated uptake of 2GPI-bound anionic surfaces in the presence of IgG anti-2GPI antibodies. Finally, 2GPI-bound oxidized LDL or activated platelets also induced the specific T-cell response. Continuous exposure to these anionic surfaces may play a critical role in maintaining the pathogenic anti-2GPI antibody response in APS patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: New therapeutic targets for antiphospholipid syndrome Tatsuya Atsumi Blood 2007 110: 4141. [Full Text] [PDF] This article has been cited by other articles: P. R. J. Ames, I. Antinolfi, A. Ciampa, J. Batuca, G. Scenna, L. R. Lopez, J. Delgado Alves, L. Iannaccone, and E. Matsuura Primary antiphospholipid syndrome: a low-grade auto-inflammatory disease? Rheumatology, December 1, 2008; 47(12): 1832 - 1837. [Abstract] [Full Text] [PDF] E Matsuura and L. Lopez Autoimmune-mediated atherothrombosis Lupus, October 1, 2008; 17(10): 879 - 888. [Abstract] [PDF]

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