Because SLE is characterized by the so-called “interferon signature” [25,26], we subsequently examined the role of type I IFNs in regulating the release of sAxl, sMer and sCD163 and looked at the effects of combining type I IFNs (IFN-α and IFN-β) with macrophage growth factors (M-CSF and GM-CSF) and/or with M2c polarizing agents (IL-10 or dexamethasone). The gene discussed is IFNA1; the disease is systemic lupus erythematosus.