TLR signaling proceeds via two pathways: the myeloid differentiation factor 88 (MyD88)-mediated pathway, and the Toll-interleukin-1 receptor (TIR)-domain-containing adaptor inducing IFN-β (TRIF)-mediated pathway [1, 2] . The former causes activation of the transcription factor NF-κB, which activates various genes contributing inflammatory reactions. The latter causes induction of IFNs, whose stimulation leads cells to antiviral state. TLR3 only activates the TRIF-mediated pathway. TLR3 signaling activates IRF-3, an important transcription factor for IFN-β, and IFN production is induced. TLR2 only activates the MyD88mediated pathway. However, TLR4 activates both pathways, so TLR4 agonists activate NF-κB and induce IFN production. Cytosolic PRRs, such as RIG-I, MDA5, and DAI, commonly activate IRF-3. The expression of PRRs differs depending on the cell type. Importantly, it is different between cells derived from myeloid stem cells (myeloid dendritic cells (mDCs), monocytes, macrophages, Langerhans cells, and neutrophils) and cells derived from lymphatic stem cells (plasmacytoid dendritic cells (pDCs), T cells, and B cells). For example, TLR7 and TLR9 are rarely expressed on mDCs, whereas TLR3 and TLR8 are rarely expressed on pDCs. TLR4, on the other hand, is expressed at very low levels on both pDCs and mDCs.