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

[1]  Y. Yamaguchi,et al.  Excessive exposure to anionic surfaces maintains autoantibody response to beta(2)-glycoprotein I in patients with antiphospholipid syndrome. , 2007, Blood.

[2]  D. Payan,et al.  R406, an Orally Available Spleen Tyrosine Kinase Inhibitor Blocks Fc Receptor Signaling and Reduces Immune Complex-Mediated Inflammation , 2006, Journal of Pharmacology and Experimental Therapeutics.

[3]  D. Arkfeld,et al.  Rituximab treatment for resistant antiphospholipid syndrome. , 2006, The Journal of rheumatology.

[4]  M. Kawai,et al.  Autoantibody to CD40 ligand in systemic lupus erythematosus: association with thrombocytopenia but not thromboembolism. , 2006, Rheumatology.

[5]  Y. Shoenfeld,et al.  International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS) , 2006, Journal of thrombosis and haemostasis : JTH.

[6]  M. Cerinic,et al.  Accelerated Atherosclerosis in Autoimmune Rheumatic Diseases , 2005, Circulation.

[7]  O. Morel,et al.  Elevated levels of procoagulant microparticles in a patient with myocardial infarction, antiphospholipid antibodies and multifocal cardiac thrombosis , 2005, Thrombosis journal.

[8]  S. Čučnik,et al.  Avidity of anti-beta-2-glycoprotein I antibodies. , 2005, Autoimmunity reviews.

[9]  T. Kveder,et al.  Budding, vesiculation and permeabilization of phospholipid membranes-evidence for a feasible physiologic role of beta2-glycoprotein I and pathogenic actions of anti-beta2-glycoprotein I antibodies. , 2005, Biochimica et biophysica acta.

[10]  Y. Ikeda,et al.  Binding of beta 2-glycoprotein I to anionic phospholipids facilitates processing and presentation of a cryptic epitope that activates pathogenic autoreactive T cells. , 2005, Blood.

[11]  J. Piette,et al.  Validation of the preliminary criteria for the classification of catastrophic antiphospholipid syndrome , 2005, Annals of the rheumatic diseases.

[12]  A. Wolberg,et al.  Mechanisms of autoantibody-induced monocyte tissue factor expression. , 2004, Thrombosis research.

[13]  G. Hughes,et al.  Circulating oxidized LDL forms complexes with beta2-glycoprotein I: implication as an atherogenic autoantigen. , 2003, Journal of lipid research.

[14]  Y. Shoenfeld,et al.  Autoantibody-mediated atherosclerosis. , 2002, Autoimmunity reviews.

[15]  K. Nitta,et al.  Antiphospholipid syndrome treated with prednisolone, cyclophosphamide and double-filtration plasmapheresis. , 2002, Internal medicine.

[16]  T. Yasuda,et al.  ω-Carboxyl variants of 7-ketocholesteryl esters are ligands for β2-glycoprotein I and mediate antibody-dependent uptake of oxidized LDL by macrophages DOI 10.1194/jlr.M20063-JLR200 , 2002, Journal of Lipid Research.

[17]  Y. Ikeda,et al.  Spleen Is a Primary Site for Activation of Platelet-Reactive T and B Cells in Patients with Immune Thrombocytopenic Purpura1 , 2002, The Journal of Immunology.

[18]  Y. Ikeda,et al.  Restricted T-cell receptor beta-chain usage by T cells autoreactive to beta(2)-glycoprotein I in patients with antiphospholipid syndrome. , 2002, Blood.

[19]  H. Inoko,et al.  Autoreactive CD4(+) T-cell clones to beta2-glycoprotein I in patients with antiphospholipid syndrome: preferential recognition of the major phospholipid-binding site. , 2001, Blood.

[20]  C. Gordon,et al.  IgG subclass distribution of antibodies against beta(2)-GP1 and cardiolipin in patients with systemic lupus erythematosus and primary antiphospholipid syndrome, and their clinical associations. , 2001, Rheumatology.

[21]  T. Yasuda,et al.  A specific ligand for beta(2)-glycoprotein I mediates autoantibody-dependent uptake of oxidized low density lipoprotein by macrophages. , 2001, Journal of lipid research.

[22]  U. Kralisz,et al.  Comparison of platelet aggregability and P-selectin surface expression on platelets isolated by different methods. , 2000, Thrombosis research.

[23]  T. Mimori,et al.  T cells that are autoreactive to beta2-glycoprotein I in patients with antiphospholipid syndrome and healthy individuals. , 2000, Arthritis and rheumatism.

[24]  G. Grau,et al.  In vitro generation of endothelial microparticles and possible prothrombotic activity in patients with lupus anticoagulant. , 1999, The Journal of clinical investigation.

[25]  M. Khamashta,et al.  Endothelial cells as target for antiphospholipid antibodies. Human polyclonal and monoclonal anti-beta 2-glycoprotein I antibodies react in vitro with endothelial cells through adherent beta 2-glycoprotein I and induce endothelial activation. , 1997, Arthritis and rheumatism.

[26]  H. Inoko,et al.  HLA-DRB4 genotyping by PCR-RFLP: diversity in the associations between HLA-DRB4 and DRB1 alleles. , 1997, Tissue antigens.

[27]  D. Alarcón-Segovia,et al.  The antiphospholipid/cofactor syndromes: a primary variant with antibodies to beta 2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays. , 1996, The American journal of medicine.

[28]  A Sali,et al.  Site-directed mutagenesis of recombinant human beta 2-glycoprotein I identifies a cluster of lysine residues that are critical for phospholipid binding and anti-cardiolipin antibody activity. , 1996, Journal of immunology.

[29]  S. Polak‐Charcon,et al.  Membranous nephropathy in primary antiphospholipid syndrome: description of a case and induction of renal injury in SCID mice. , 1996, Human antibodies and hybridomas.

[30]  A. Lanzavecchia,et al.  Modulation of antigen processing by bound antibodies can boost or suppress class II major histocompatibility complex presentation of different T cell determinants , 1995, The Journal of experimental medicine.

[31]  Y. Shoenfeld,et al.  Immunization with anticardiolipin cofactor (beta-2-glycoprotein I) induces experimental antiphospholipid syndrome in naive mice. , 1994, Journal of autoimmunity.

[32]  J. Hunt,et al.  The fifth domain of beta 2-glycoprotein I contains a phospholipid binding site (Cys281-Cys288) and a region recognized by anticardiolipin antibodies. , 1994, Journal of immunology.

[33]  T. Sumida,et al.  Heterogeneity of anticardiolipin antibodies defined by the anticardiolipin cofactor. , 1992, Journal of immunology.

[34]  T. Barbui,et al.  Anticardiolipin antibodies (ACA) directed not to cardiolipin but to a plasma protein cofactor , 1990, The Lancet.

[35]  C. Chesterman,et al.  Anti-phospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation: beta 2-glycoprotein I (apolipoprotein H). , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[36]  G. Hughes,et al.  Thrombosis, recurrent fetal loss, and thrombocytopenia. Predictive value of the anticardiolipin antibody test. , 1986, Archives of internal medicine.

[37]  H. Wurm.  beta 2-Glycoprotein-I (apolipoprotein H) interactions with phospholipid vesicles. , 1984, The International journal of biochemistry.