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Background and aims: Systemic lupus erythematosus (SLE) is a chronic multi-organ autoimmune disease with immunological features of a prominent "interferon (IFN) signature", which is marked by the elevated expression of type Ⅰ IFNregulated genes in blood and tissue cells of patients with this condition.Plasmacytoid dendritic cells (pDCs), the most potent type Ⅰ IFN-producing cells, are previously found to be hyperactive in SLE.Using the New Zealand Black/White F 1 lupus mouse model, the current study sought for the regulatory mechanism of IFN production by pDCs in SLE.