Toll-like receptor signal transduction and the tailoring of innate immunity: a role for Mal?

Recent evidence suggests that there may be specificities in the signal transduction pathways activated by different Toll-like receptors (TLRs), with different sets of genes being induced by TLR-4 when compared with TLR-2. These differences may be because of different signalling adapters, with MyD88 being used by several TLRs, and the adapter MyD88-adapter-like (Mal) being recruited specifically by TLR-4. The set of genes being induced may be tailored for the subsequent elimination of the pathogen being recognized, as a result of differences in signal transduction pathways activated by TLRs. These findings may ultimately explain how dendritic cells control specific T-cell responses.