Invariant Natural Killer T Cells Promote T Cell Immunity by Modulating the Function of Lung Dendritic Cells during Chlamydia pneumoniae Infection

被引:14
|
作者
Shekhar, Sudhanshu [1 ]
Joyee, Antony George [2 ]
Gao, Xiaoling [1 ]
Peng, Ying [1 ]
Wang, Shuhe [1 ]
Yang, Jie [1 ]
Yang, Xi [1 ,2 ]
机构
[1] Univ Manitoba, Fac Med, Dept Med Microbiol, Lab Infect & Immun, Winnipeg, MB R3E 0T5, Canada
[2] Univ Manitoba, Fac Med, Dept Immunol, Winnipeg, MB R3E 0T5, Canada
基金
加拿大健康研究院;
关键词
Invariant natural killer T cells; Lung dendritic cells; T cells; Chlamydia pneumoniae; IFN-GAMMA; NKT CELLS; RESPONSES; SUBSETS; ACTIVATION; INDUCTION; MOLECULES; ANTIGENS; INNATE; IL-10;
D O I
10.1159/000368779
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study, we examined the effect of invariant natural killer T (iNKT) cells on the function of lung dendritic cells (LDCs) in eliciting protective immunity against Chlamydia pneumoniae (Cpn) lung infection. We employed a combination of approaches including the use of iNKT cell-deficient, J alpha 18-knockout (KO) mice and LDC adoptive transfer. We found that iNKT cells significantly altered the number, phenotype and cytokine profile of LDCs following infection. Furthermore, coculture of T cells with LDCs from Cpn-infected wildtype (WT) and KO mice induced type-1 and type-2 responses, respectively. More importantly, upon adoptive transfer, LDCs from Cpn-infected WT mice (WT-LDCs) conferred protective immunity, whereas LDCs from KO mice (KO-LDCs) increased the severity of disease after challenge infection. Further cytokine analyses of the lung tissues and lung-draining lymph node cells showed that KO-LDC-recipient mice exhibited a type-2 cytokine production pattern, while WT-LDC recipients exhibited a type-1 cytokine profile. Taken together, our results provide in vivo evidence that iNKT cells play a critical role in modulating LDC function to generate protective T-cell immunity, particularly in a clinically relevant intracellular bacterial infection. (C) 2014 S. Karger AG, Basel
引用
收藏
页码:260 / 274
页数:15
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