Immunodeficiency: UNC-93B gets a toll call

Defects in innate immunity have moved to center stage in the past five years. This can be explained, at least in part, by the development of molecular assays and genetic tools that enable new approaches. Two recent studies using these elegant tools show that a transmembrane endoplasmic reticulum protein, UNC-93B, is essential for the normal response to signaling through the Toll-like receptors (TLRs) that respond to viral infection, TLR3, TLR7, TLR8 and TLR9.