Cutting edge: TLR ligands increase TCR triggering by slowing peptide-MHC class I decay rates

Brian D. Rudd, James D. Brien, Miles P. Davenport, Janko Nikolich-Žugich

Research output: Contribution to journalArticle

13 Scopus citations


TLR ligands are among the key stimuli driving the optimal dendritic cell (DC) maturation critical for strong and efficacious T cell priming. In this study, we show that part of this effect occurs via increased TCR triggering. Pretreatment of DCs with TLR ligands resulted in the triggering of many more TCRs in responding CD8+ T cells. Importantly, even when DCs expressed the same amount of cognate peptide-MHC (pMHC) molecules, TLR ligand treatment resulted in down-regulation of larger numbers of TCR molecules. This was independent of the up-regulation of costimulatory, adhesion or cytokine molecules or the amount of noncognate pMHCs. Rather, DCs pretreated with TLR ligands exhibited increased stability of cognate pMHCs, enabling extended TCR triggering. These findings are of potential importance to T cell vaccination.

Original languageEnglish (US)
Pages (from-to)5199-5203
Number of pages5
JournalJournal of Immunology
Issue number8
StatePublished - Jan 1 2008


ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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