A human ortholog of SIGN-R1, DC-SIGN, was also able to bind sFc ex vivo (10), and the protective activity of sFc and sialylated IVIg (sIVIg) was retained upon induction of arthritis in SIGN-R1−/− mice that transgenically expressed human DC-SIGN (13). The gene discussed is CD209; the disease is arthritic joint disease.