Among these factors, programmed death ligand 1 in combination with TGF-β is particularly important for promoting the conversion of CD4+ T cells to Foxp3+ CD4+ Treg cells, whereas blockade of programmed death ligand 1 can reduce anti-dsDNA IgG production and immune-complex formation in lupus-prone mice by suppressing the synthesis of IL-10 in CD4+ Treg and B cells, thus further validating the therapeutic potential of iDCs (128, 129). The gene discussed is FOXP3; the disease is systemic lupus erythematosus.