Using a murine model of arthritis, it has been shown that targeting the DC C-type lectin (DC-SIGN) on DC or bone marrow derived macrophages with IVIg can induce IL-4 production by basophils, leading to increased levels of the inhibitory receptor FcγRIIB on macrophages, which the group suggested may provide a mechanism for maintaining immune homeostasis [12]. The gene discussed is IL4; the disease is arthritic joint disease.