Introduction
Systemic lupus erythematosus (SLE) is a multisystem
disorder that is considered a prototype immune
complex (IC)-mediated disease.1 It is virtually
always accompanied by autoantibodies against
nuclear constituents, e.g. against double-stranded
(ds) DNA, Sjo¨ gren’s syndrome A (SSA) and B
(SSB), U1-snRNP and Sm antigens. Whereas
levels of antibodies against dsDNA co-vary with