Nasal-associated lymphoid tissues (NALTs) support the recall but not priming of influenza virus-specific cytotoxic T cells

Nasal-associated lymphoid tissues (NALTs) support the recall but not priming of influenza virus-specific cytotoxic T cells
复制标题

DOI:
10.1073/pnas.1620194114
复制
发表时间:
2017-05-16
影响因子:
11.1
通讯作者:
Wakim, Linda M.
Wakim, Linda M.
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Pizzolla, Angela;Wang, Zhongfang;Wakim, Linda M.

文献摘要

被引文献

相似文献

排入上呼吸道的淋巴组织是细胞毒性T淋巴细胞(CTL)对空气传播病原体和鼻内疫苗免疫的重要诱导位点。在这里,我们研究了鼻相关淋巴组织(NALTs)在上呼吸道感染致病性流感病毒和接种减毒流感病毒活疫苗后CD8(+) T细胞初始启动和召回扩增中的作用。NALTs是嵌入鼻腔粘膜下层的粘膜相关淋巴器官。尽管NALTs在流感病毒感染或疫苗接种后作为记忆性CD8(+) T细胞回忆扩增的诱导位点,但它们不能支持初始CD8(+) T细胞的激活。引人注目的是,与其他淋巴组织不同,NALTs在稳定状态下没有通过循环T细胞进行常规调查。当感染诱导趋化因子CXCL10升高时,记忆性T细胞选择性募集到这些淋巴结构中,这吸引了CXCR3(+)记忆性CD8(+) T细胞。这些结果对鼻内疫苗具有重要意义,该疫苗可将抗原递送到粘膜相关淋巴组织,并旨在引发保护性ctl介导的免疫。
The lymphoid tissue that drains the upper respiratory tract represents an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathogens and intranasal vaccines. Here, we investigated the role of the nasal-associated lymphoid tissues (NALTs), which are mucosal-associated lymphoid organs embedded in the submucosa of the nasal passage, in the initial priming and recall expansion of CD8(+) T cells following an upper respiratory tract infection with a pathogenic influenza virus and immunization with a live attenuated influenza virus vaccine. Whereas NALTs served as the induction site for the recall expansion of memory CD8(+) T cells following influenza virus infection or vaccination, they failed to support activation of naive CD8(+) T cells. Strikingly, NALTs, unlike other lymphoid tissues, were not routinely surveyed during the steady state by circulating T cells. The selective recruitment of memory T cells into these lymphoid structures occurred in response to infection-induced elevation of the chemokine CXCL10, which attracted CXCR3(+) memory CD8(+) T cells. These results have significant implications for intranasal vaccines, which deliver antigen to mucosal-associated lymphoid tissue and aim to elicit protective CTL-mediated immunity.