Although it is unlikely that the increased IL-10 synthesis in TLR3-deficient mice impacts the C. muridarum-induced IFN-β synthesized early during infection (that we have shown to be mostly TLR3 dependent in OE cells), its synthesis more likely suppresses IFN-β secreted from pathways other than TLR3, which are mostly IFN-β amplification pathways that are active in the cell late during infection [68]. Here, TLR3 is linked to infection.