Rheumatology 2001; 40: 1026-1032
© 2001 British Society for Rheumatology
Original Papers |
IgG subclass distribution of antibodies against ß2-GP1 and cardiolipin in patients with systemic lupus erythematosus and primary antiphospholipid syndrome, and their clinical associations
5th Department of Internal Medicine, Evangelismos Hospital, Athens, Greece,
1 Rheumatology Section, Division of Medicine, Hammersmith Hospital, Imperial College School of Medicine, London and
2 Department of Rheumatology, Division of Immunity and Infection, University of Birmingham, Birmingham, UK
Objectives. To determine the immunoglobulin G (IgG) subclass distribution of anticardiolipin (aCL) and anti-ß2-glycoprotein 1 (ß2-GP1) antibodies (aß2-GP1), and to examine possible associations between the different aß2-GP1 and aCL subclasses and the main clinical manifestations of the antiphospholipid syndrome (APS).
Methods. We studied 130 patients with systemic lupus erythematosus and 35 patients with primary APS. We used enzyme-linked immunosorbent assays to measure IgG aCL and aß2-GP1 and to determine the IgG subclass distribution of these two autoantibodies.
Results. When the number of patients positive for each subclass was examined, IgG3 and IgG2 aCL were more frequent (63.5 and 54.1% of patients were positive for the two subclasses, respectively), while for aß2-GP1 IgG2 was the most prevalent subclass (81.8% of patients were positive). IgG2 aCL was significantly associated with arterial thrombosis (P=0.023) and fetal loss (P=0.013), and IgG3 aCL was significantly associated with arterial thrombosis (P=0.0003) and fetal loss (P=0.045). IgG2 aß2-GP1 was associated with venous thrombosis (P=0.012) and IgG3 aß2-GP1 was associated with venous thrombosis (P=0.036) and fetal loss (P=0.024).
Conclusions. The IgG2 predominance of aß2-GP1 suggests that the antibody response against ß2-GP1 may be T-cell-independent. As IgG2 and IgG3 differ in their effector functions, their association with the same clinical manifestations (i.e. thrombosis and fetal loss) suggests that more than one mechanism may be involved in the pathogenesis of thrombosis and fetal loss in APS.
KEY WORDS: Systemic lupus erythematosus, Anticardiolipin/antiphospholipid antibodies, IgG subclasses.
Correspondence to: M. Samarkos, 5th Department of Internal Medicine, Evangelismos Hospital, 45–47 Ipsilantou Street, Athens 10676, Greece.
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