This seems also to be the case in humans, as complementary findings were made in healthy volunteers bearing a loss-of-function variant in FCGR2B. The proportion of IGHV4-34 clones, known to be autoreactive, was significantly higher in the activated CD19+IgD−CD27−CD38mid/hi and CD19+IgD+CD27+ B-cell subsets in individuals homozygous for the FCGR2B T232 loss-of-function SLE-associated polymorphism. Here, CD19 is linked to systemic lupus erythematosus.