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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 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 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 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 Free Research Articles Hemostasis, Thrombosis, and Vascular Biology Immunobiology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Excessive exposure to anionic surfaces maintains autoantibody response to β2-glycoprotein I in patients with antiphospholipid syndrome Yukie Yamaguchi1,2, Noriyuki Seta1, Junichi Kaburaki3, Kazuko Kobayashi4, Eiji Matsuura4, and Masataka Kuwana1 1 Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo; 2 Department of Environmental Immuno-dermatology, Yokohama City University Graduate School of Medicine, Yokohama; 3 Department of Internal Medicine, Tokyo Electric Power Company Hospital, Tokyo; and 4 Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Antiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder associated with autoantibodies to phospholipid (PL)–binding proteins, such as β2-glycoprotein I (β2GPI). We have recently reported that binding of β2GPI to anionic PL facilitates processing and presentation of the cryptic β2GPI epitope that activates pathogenic autoreactive T cells. To clarify mechanisms that induce sustained presentation of the dominant antigenic β2GPI determinant in patients with APS, T-cell proliferation induced by β2GPI-treated phosphatidylserine liposome (β2GPI/PS) was evaluated in bulk peripheral blood mononuclear cell cultures. T cells from patients with APS responded to β2GPI/PS in the presence of immunoglobulin G (IgG) anti-β2GPI 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 β2GPI-bound anionic surfaces in the presence of IgG anti-β2GPI antibodies. Finally, β2GPI-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-β2GPI antibody response in patients with APS. 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]

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