Since we have demonstrated that hCDR1 was capable of restoring the cytokine dysregulation observed in SLE and of down regulating the maturation and function of dendritic cells (that are activated by IFN-α and are a source for IFN-α production as well) we investigated, in the present studies, the effects of hCDR1 on IFN-α in a murine model of SLE and in human lupus. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.