Excessive exposure to anionic surfaces maintains autoantibody response to β2-glycoprotein I in patients with antiphospholipid syndrome

Yukie Yamaguchi, Noriyuki Seta, Junichi Kaburaki, Kazuko Kobayashi, Eiji Matsuura, Masataka Kuwana

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)


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 (β 2GPI/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-FcγRI antibody. These findings indicate that efficient presentation of the cryptic determinants can be achieved by monocytes undergoing FcγRI-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.

Original languageEnglish
Pages (from-to)4312-4318
Number of pages7
Issue number13
Publication statusPublished - Dec 15 2007

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology


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