The role of Akt in nicotine regulating dendritic cell cross presentation
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- 英文论文题名：The role of Akt in nicotine regulating dendritic cell cross presentation
- 论文作者：Hu chunfang ; Xu dandan ; Gao fengguang
- 英文论文作者：Hu chunfang ; Xu dandan ; Gao fengguang ; Department of Immunology ; Basic Medicine Science ; Medical College ; Xiamen University ; State Key Laboratory of Oncogenes and Related Genes ; Shang Hai Jiao Tong University
- 年：2016
- 作者机构：Department of Immunology,Basic Medicine Science,Medical College,Xiamen University;State Key Laboratory of Oncogenes and Related Genes,Shang Hai Jiao Tong University;
- 英文论文关键词：Akt ; nicotine ; cross presentation ; dendtric cells
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R392
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：352k
- 原文格式：D
- 会议级别：全国
摘要
Objectives: Mannose receptor mediating endocytosis and endosomal recruitment of antigen play important roles in dendritic cells(DCs) cross presentation. Our previous study showed that the treatment with nicotine obviously augment DCs cross presentation and efficiently activate Akt pathway, but the exact roles of Akt in nicotine mediating endocytosis and endosomal recruitment of antigen are still unclear.Methods: DCs were derived from bone marrow precursor cells cultured with GM-CSF and IL-4. Then, the cells were stimulated with nicotine and the effects of nicotine on mannose receptor(MR) expression and Akt pathway activation were determinated by western blot. Akt pathway inhibitors or siRNA were further applied to inhibit the effect of nicotine on Akt activation and the role of Akt in nicotine regulating MR up-regulation, endocytosis and endosomal recruitment of antigen was observed by western blot, laser confocal microscopy and co-immunoprecipitation(co-IP). Finally, the actor of Akt in nicotine increased cross-presentation and cross-priming were investigated by confocal and Elispot respectively.Results: Firstly, Nicotine increase the expression of MR and up-regulate phosphorylation of Akt. Additionally,the inhibition of Akt abolished the nicotine's effect on MR expression. Secondly, the obvious colocalization of of Akt and MR was verified by Laser confocal microscopy and co-IP repectively. Thirdly, the inhibition of Akt efficiently increase the colocalization of antigen peptide-MHC I complexes with early endosome markers.Fourthly, the role of Akt in nicotine regulating cross-priming were further confirmed by Enzyme linked immunospot assay.Conclusions: Nicotine increase the expression of MR through Akt activation. However, Akt linked to MR decrease endocytosis and endosomal recruitment of antigen, result in attenuate cross presentation and cross priming, indicating an significant but complicated role of Akt plays in nicotine-augmented cross-presentation.
Objectives: Mannose receptor mediating endocytosis and endosomal recruitment of antigen play important roles in dendritic cells(DCs) cross presentation. Our previous study showed that the treatment with nicotine obviously augment DCs cross presentation and efficiently activate Akt pathway, but the exact roles of Akt in nicotine mediating endocytosis and endosomal recruitment of antigen are still unclear.Methods: DCs were derived from bone marrow precursor cells cultured with GM-CSF and IL-4. Then, the cells were stimulated with nicotine and the effects of nicotine on mannose receptor(MR) expression and Akt pathway activation were determinated by western blot. Akt pathway inhibitors or siRNA were further applied to inhibit the effect of nicotine on Akt activation and the role of Akt in nicotine regulating MR up-regulation, endocytosis and endosomal recruitment of antigen was observed by western blot, laser confocal microscopy and co-immunoprecipitation(co-IP). Finally, the actor of Akt in nicotine increased cross-presentation and cross-priming were investigated by confocal and Elispot respectively.Results: Firstly, Nicotine increase the expression of MR and up-regulate phosphorylation of Akt. Additionally,the inhibition of Akt abolished the nicotine's effect on MR expression. Secondly, the obvious colocalization of of Akt and MR was verified by Laser confocal microscopy and co-IP repectively. Thirdly, the inhibition of Akt efficiently increase the colocalization of antigen peptide-MHC I complexes with early endosome markers.Fourthly, the role of Akt in nicotine regulating cross-priming were further confirmed by Enzyme linked immunospot assay.Conclusions: Nicotine increase the expression of MR through Akt activation. However, Akt linked to MR decrease endocytosis and endosomal recruitment of antigen, result in attenuate cross presentation and cross priming, indicating an significant but complicated role of Akt plays in nicotine-augmented cross-presentation.
Objectives: Mannose receptor mediating endocytosis and endosomal recruitment of antigen play important roles in dendritic cells(DCs) cross presentation. Our previous study showed that the treatment with nicotine obviously augment DCs cross presentation and efficiently activate Akt pathway, but the exact roles of Akt in nicotine mediating endocytosis and endosomal recruitment of antigen are still unclear.Methods: DCs were derived from bone marrow precursor cells cultured with GM-CSF and IL-4. Then, the cells were stimulated with nicotine and the effects of nicotine on mannose receptor(MR) expression and Akt pathway activation were determinated by western blot. Akt pathway inhibitors or siRNA were further applied to inhibit the effect of nicotine on Akt activation and the role of Akt in nicotine regulating MR up-regulation, endocytosis and endosomal recruitment of antigen was observed by western blot, laser confocal microscopy and co-immunoprecipitation(co-IP). Finally, the actor of Akt in nicotine increased cross-presentation and cross-priming were investigated by confocal and Elispot respectively.Results: Firstly, Nicotine increase the expression of MR and up-regulate phosphorylation of Akt. Additionally,the inhibition of Akt abolished the nicotine's effect on MR expression. Secondly, the obvious colocalization of of Akt and MR was verified by Laser confocal microscopy and co-IP repectively. Thirdly, the inhibition of Akt efficiently increase the colocalization of antigen peptide-MHC I complexes with early endosome markers.Fourthly, the role of Akt in nicotine regulating cross-priming were further confirmed by Enzyme linked immunospot assay.Conclusions: Nicotine increase the expression of MR through Akt activation. However, Akt linked to MR decrease endocytosis and endosomal recruitment of antigen, result in attenuate cross presentation and cross priming, indicating an significant but complicated role of Akt plays in nicotine-augmented cross-presentation.
引文