In addition to the above ISGs, MoDCs of XLA patients failed to up-regulate the expression of IRF7 and TLR3 in response to OPV, while OPV failed to induce IRF3 expression in MoDCs of both XLA patients and healthy controls (Figure 5), possibly because IRF3 is constitutively expressed in all dendritic cell types and its expression cannot be further stimulated by IFN-α (31, 32). The gene discussed is IFNA2; the disease is Bruton-type agammaglobulinemia.