Low copy number (CN) of theFCGR3Bgene reducesFCGR3Bmembrane expression on neutrophils and results in clearance of a smaller amount of immune complex. We investigatedFCGR3BCN in relation to the clinical phenotype in a Caucasian SLE cohort ().FCGR3BCN was determined by three different qPCR parameter estimations (Ct−, Cy0, and cpD1) and confirmed by the FCGR2C/FCGR2A paralog ratio test. Clinical and serological data were then analyzed for their association withFCGR3BCN. LowFCGR3BCN (<2) was more frequent in SLE patients than in healthy controls () (20% versus 6%, OR 4.15, ) and associated with higher disease activity scores (SLEDAI 10.4 versus 6.1, ), lupus nephritis (LN) (25 versus 5%, ), and increased levels of antibodies against dsDNA (81 versus 37 IU, ), C1q (22 versus 6 IU, ), and ribosomal P (10 versus 5 IU, ). No such associations were seen with antibodies against extractable nuclear antigens or highFCGR3BCN (>2). In multivariate analyses, LN was independently associated with anti-C1q-Ab levels () and lowFCGR3BCN (). We conclude that the susceptibility for LN in patients with lowFCGR3BCN is linked to increased levels of pathogenic autoantibodies.
Antibodies to ribosomal P proteins in lupus nephritis: A surrogate marker for a better renal survival?
