Neutrophils with fewer copies of FCGR3B bind poorly to IgG complexes.
Cells can have as many as four copies of this gene, FCGR3B, which encodes the FcγRIIIb receptor, but some lupus patients have fewer than two. Willcocks et al. now find that this scarcity leads to fewer receptors on neutrophils, which thus fail to bind and destroy inflammation-causing antibody clusters. The paucity of receptors did not impair other neutrophil functions such as the production of oxygen radicals.
Some healthy individuals also had fewer copies of the gene and thus similarly defective neutrophils. But these individuals do not develop lupus, most likely because they lack other genetic defects required to cause disease. The compensatory influence of other genes might also explain why low copy number of FCGR3B is not a risk factor for lupus among all populations.
Having more FcγRIIIb receptors, however, doesn't guarantee good health. The group found that a high copy number of FCGR3B was associated with vasculitis—a disease in which neutrophils release damaging oxygen radicals in response to cross-linking of FcγRIIIb receptors on blood vessel walls. 
