期刊
ONCOTARGET
卷 7, 期 25, 页码 38451-38466出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9498
关键词
mannose receptor; cross-presentation; alpha 7 nicotinic acetylcholine receptor; dendritic cells; toll-like receptor 4
资金
- State Key Laboratory of Oncogenes and Related Genes [90-14-05]
- National Natural Science Foundation of China [81273203]
Cross-presentation by dendritic cells (DCs) requires surface molecules such as lectin, CD40, langerin, heat shock protein, mannose receptor, mediated endocytosis, the endosomal translocation of internalized antigen, and the relocation of transporter associated with antigen processing (TAP). Although the activation of alpha 7 nicotinic acetylcholine receptor (alpha 7 nAchR) up-regulate surface molecule expression, augment endocytosis, and enhance cross-presentation, the molecular mechanism of alpha 7 nAchR activation-increased cross-presentation is still poorly understood. In this study, we investigated the role of mannose receptor in nicotine-increased cross-presentation and the mechanism that endotoxins orchestrating the recruitment of TAP toward endosomes. We demonstrated that nicotine increase the expressiones of mannose receptor and Toll-like receptor 4 (TLR4) via PI3K-Akt-mTOR-p70S6 pathway. Both endosomal translocation of mannose receptor-internalized antigens and TLR4 signaling are necessary for nicotine-augmented cross-presentation and cross-priming. Importantly, the recruitment of TAP toward endosomes via TLR4-MyD88-IRAK4 signaling contributes to nicotine-increased cross-presentation and cross-activation of T cells. Thus, these data suggest that increased recruitment of TAP to Ag-containing vesicles contributes to the superior cross-presentation efficacy of alpha 7 nAchR activated DCs.
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