A potential protective mechanism of pDCs may be driven by induction of a tolerogenic phenotype in APCs by the Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA-4), through increased production of indoleamine 2,3-deoxygenase, allowing these cells to induce the conversion of naïve T cells into Treg cells.22 Like we have found in AIH, a reduced frequency of circulating pDCs was described in patients with acute and chronic viral hepatitis B and C23,24. This evidence concerns the gene CTLA4 and autoimmune hepatitis.