Immunity
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Toll-like receptors (TLRs) play prominent roles in initiating immune responses to infection, but their roles in particular cell types in vivo are not established. Here we report the generation of mice selectively lacking the crucial TLR-signaling adaptor MyD88 in dendritic cells (DCs). ⋯ Whereas the innate interferon-gamma response of natural killer cells and of natural killer T cells and the Th1 polarization of antigen-specific CD4(+) T cells were severely compromised after treatment with a soluble TLR9 ligand, they were largely intact after administration of an aggregated TLR9 ligand. These results demonstrate that the physical form of a TLR ligand affects which cells can respond to it and that DCs and other innate immune cells can respond via TLRs and collaborate in promoting Th1 adaptive immune responses to an aggregated stimulus.
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In this issue of Immunity, Hou et al. (2008) describe the generation of mice that selectively lack the adaptor protein MyD88 in dendritic cells (DCs). These mice demonstrate that the requirement for Toll-like receptor (TLR) signaling in DCs is dependent on the physical form of the TLR ligand.