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Immunity. 2008 Aug 15;29(2):272-82. doi: 10.1016/j.immuni.2008.05.016. Epub 2008 Jul 24.

Toll-like receptors activate innate and adaptive immunity by using dendritic cell-intrinsic and -extrinsic mechanisms.

Author information

  • 1Department of Microbiology & Immunology, University of California, San Francisco, CA, 94143, USA.

Abstract

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). In these mice, the early production of inflammatory cytokines, especially IL-12, was substantially reduced after TLR stimulation. 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.

Comment in

  • 2008: A MyD88 O, DC. [Immunity. 2008]
PMID:
18656388
[PubMed - indexed for MEDLINE]
PMCID:
PMC2847796
Free PMC Article

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