Binding of complement component C1q to anti- β 2 glycoprotein I antibodies from patients with antiphospholipid syndrome

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Abstract
Objective: To determine if anti-β 2 GPI reactive with surface-bound β 2 GPI can bind C1q, i.e. to determine whether surface-bound β 2 GPI-anti-β 2 GPI immune complexes can initiate the classical pathway of complement activation.¶Methods: β 2 GPI was bound to chemically-activated microtiter plates which had previously been shown to promote anti-β 2 GPI reactivity with bound β 2 GPI. Wells with surface-bound β 2 GPI (capped with bovine serum albumin) were then reacted with complement-inactivated sera from antiphospholipid syndrome patients (APS) or with control sera. Following removal of unbound serum components, the wells were incubated with biotinylated C1q and probed with peroxidase-conjugated avidin D. Bound C1q was detected at 450nm using tetramethyl benzidine/peroxidase as a substrate system and expressed as absorbance units (Abs).¶Results: The identified 20 APS with elevated anti-β 2 GPI: 4 with IgG only, 4 with IgM only, 1 with IgA only, 1 with IgG and IgA, 6 with IgG and IgM and 4 with IgG, IgA and IgM. C1q binding from 20 healthy controls was 0.039 ± 0.029 (SD). Of the APS, 17/20 (85%) had Abs >5 SD above controls. The 3 APS with C1q Abs within normal limits had, respectively, IgM only (1), IgA only (1), and both IgG and IgM (1). Statistical analyses (Kruskal-Wallis followed by Dunn's post test) suggest differences in IgG and IgG + IgM groups compared to con (Kruskal-Wallis: p = 0.0002; Dunn's: con vs. IgG, p < 0.05; con vs. IgG + IgM, p < 0.01). ¶Conclusions: Anti-β 2 GPI from APS appear to have a variable degree of C1q affinity. Those patients with strong C1q binding responses are likely to have an inflammatory component to their disease processes.

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