TLR3 and infection: First, the authors followed the response to infection in a strain of mice called 3d, which has a loss-of-function point mutation in UNC93B1 (an endoplasmic reticulum (ER) resident protein that mediates the translocation of the nucleotide-sensing TLRs from the ER to the endolysosomes) and, consequently, is unresponsive to TLR3, TLR7 and TLR9 ligands (TLR8 is believed to be biologically inactive in mice).