Anti-C1q
antibodies are prevalent in patients with active
lupus nephritis and were found to be closely associated with renal involvement and predictive for a flare of
nephritis. However, the pathogenesis of anti-C1q
antibodies involved in human
lupus nephritis remains unclear. C1q, which plays a key role in apoptotic cell and
immune complex removal, is a very important functional molecule in the pathogenesis of SLE. The aim of this study was to investigate the influence of anti-C1q
autoantibodies from active
lupus nephritis patients on the bio-functions of C1q in vitro. We purified
IgG autoantibodies against C1q from
lupus nephritis patients, and found that they could recognize C1q bound on early apoptotic cells at 30 μg/ml, and could significantly decrease the phagocytosis by macrophages of early apoptotic cells opsonized by 50 μg/ml C1q in comparison with normal
IgG. Levels of circulating
immune complexes of the ten patients were measured by a circulating
immune complexes (CIC)-C1q
Enzyme Immunoassay Kit. Anti-C1q
autoantibodies affinity purified by microtiter plates could significantly inhibit the deposition of C3c on CIC-C1q in a dose dependent manner in comparison with
IgG from 10 healthy blood donors. The binding of opsonized
immune complexes to RBCs was significantly inhibited by anti-C1q
autoantibodies purified by microtiter plates in a dose dependent manner. Our observations suggest that serum anti-C1q
autoantibodies from active
lupus nephritis patients could interfere with some biological function of C1q in vitro.