The Role of Invariant Natural Killer T Cells in Dendritic Cell Licensing, Cross-Priming, and Memory CD8(+) T Cell Generation.

The Role of Invariant Natural Killer T Cells in Dendritic Cell Licensing, Cross-Priming, and Memory CD8(+) T Cell Generation.
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DOI:
10.3389/fimmu.2015.00379
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发表时间:
2015
影响因子:
7.3
通讯作者:
Kurts C
Kurts C
中科院分区:
医学2区
文献类型:
--
作者:
Gottschalk C;Mettke E;Kurts C

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新的疫苗接种策略侧重于实现CD8+ T细胞(CTL)免疫,而不是诱导保护性抗体反应。虽然CD4+ T (Th)细胞的需求有助于树突状细胞(DC)的激活和许可,以及CTL记忆的诱导已经在几种疾病模型中被描述,但CTL反应可能以Th细胞独立的方式发生。不变性自然杀伤T细胞(iNKT细胞)也可以代替T细胞帮助和许可DC。iNKT细胞产生广谱的Th1和Th2细胞因子,从而在DC中诱导类似的共刺激分子和细胞因子。这种许可形式不同于Th细胞通过诱导其他趋化因子来帮助,而Th细胞许可的dc产生CCR5配体,iNKT细胞许可的dc产生CCL17, CCL17吸引CCR4+ CD8+ T细胞进行随后的激活。最近的研究表明,iNKT细胞不仅可以增强对细菌病原体或寄生虫的免疫反应,而且还可以在病毒感染中发挥作用。在小鼠模型中,在流感病毒疫苗中包含iNKT细胞配体增强了记忆CTL的产生和保护性免疫。本文将重点讨论iNKT细胞在交叉启动DC和记忆CD8+ T细胞形成的串扰中的作用。
New vaccination strategies focus on achieving CD8+ T cell (CTL) immunity rather than on induction of protective antibody responses. While the requirement of CD4+ T (Th) cell help in dendritic cell (DC) activation and licensing, and in CTL memory induction has been described in several disease models, CTL responses may occur in a Th cell help-independent manner. Invariant natural killer T cells (iNKT cells) can substitute for Th cell help and license DC as well. iNKT cells produce a broad spectrum of Th1 and Th2 cytokines, thereby inducing a similar set of costimulatory molecules and cytokines in DC. This form of licensing differs from Th cell help by inducing other chemokines, while Th cell-licensed DCs produce CCR5 ligands, iNKT cell-licensed DCs produce CCL17, which attracts CCR4+ CD8+ T cells for subsequent activation. It has recently been shown that iNKT cells do not only enhance immune responses against bacterial pathogens or parasites but also play a role in viral infections. The inclusion of iNKT cell ligands in influenza virus vaccines enhanced memory CTL generation and protective immunity in a mouse model. This review will focus on the role of iNKT cells in the cross-talk with cross-priming DC and memory CD8+ T cell formation.