title: Reactivities of antiphospholipid antibodies to blood cells and their effects on platelet aggregations in vitro.
abstract: To clarify the pathogenesis of antiphospholipid antibody (aPL) syndrome, the reactivities of anticardiolipin antibodies (aCL) in sera of patients with systemic lupus erythematosus (SLE) or other diseases to fresh, activated or destroyed blood cells were examined by the inhibition assay using an enzyme-linked immunosorbent assay. In addition, the effects of lupus anticoagulants (LA) in the patients' plasma and of immune complexes formed between LA and PL antigens on platelet aggregations were also determined. The IgG-aCL activity of patients' sera was markedly inhibited by pre-incubation with freeze-thawed blood cells, including erythrocytes (RBC), mononuclear cells (MNC) and platelets, but not fresh platelets or RBC. The aCL activity was slightly inhibited by fresh MNC, and was definitely inhibited by thrombin-activated platelets and polymorphonuclear cells (PMN) stimulated with phorbol 12-myristate 13-acetate (PMA). However, the activity was not inhibited by platelets stimulated with adenosine 5'-diphosphate (ADP; 10 microM). Twenty-two LA positive plasma and 17 LA negative plasma from patients similarly enhanced the aggregation of platelets which were obtained from healthy adults and stimulated with low concentrations of ADP (1 or 2 microM). However, such enhancement of platelet aggregation was not observed when high concentrations of ADP (5 microM) or collagen (2 micrograms/ml) were used as stimulators. In four of the 16 LA positive plasma examined, the mixture of plasma and phospholipid reagent for activated partial thromboplastin time induced platelet aggregations without the other stimulations, but the plasmas themselves did not induce such a reaction. The above results indicate that the aPL from patients do not react with intact blood cells in vitro, but they can react with activated or destroyed blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Department of Internal Medicine, School of Medicine, Tokai University, Japan.
authors: Y
authors: Y
authors: Ichikawa
authors: N
authors: N
authors: Kobayashi
authors: T
authors: T
authors: Kawada
authors: H
authors: H
authors: Shimizu
authors: J
authors: J
authors: Moriuchi
authors: H
authors: H
authors: Ono
authors: K
authors: K
authors: Watanabe
authors: S
authors: S
authors: Arimori
mesh_terms: D000906:Antibodies / Q000502:physiology*; D001773:Blood Cells / Q000502:physiology*; D001779:Blood Coagulation Factors / Q000276:immunology / Q000502:physiology; D002308:Cardiolipins / Q000276:immunology; D006801:Humans; D016682:Lupus Coagulation Inhibitor; D008180:Lupus Erythematosus, Systemic / Q000097:blood; D010743:Phospholipids / Q000276:immunology*; D015539:Platelet Activation; D010974:Platelet Aggregation
chemical_list: D000906:Antibodies; D001779:Blood Coagulation Factors; D002308:Cardiolipins; D016682:Lupus Coagulation Inhibitor; D010743:Phospholipids