期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 8, 页码 5199-5203出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.8.5199
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类别
资金
- U.S. Public Health Service [AI-066096]
- Oregon National Primate Research Center [RR-0163]
- National Institute of Allergy and Infectious Diseases
- National Center for Research Resources
- National Institutes of Health
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.
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