Rapid development of a gamma interferon-secreting glycolipid/CD1d-specific Vα14+ NK1.1- T-cell subset after bacterial infection
Rapid development of a gamma interferon-secreting glycolipid/CD1d-specific Vα14+ NK1.1- T-cell subset after bacterial infection
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DOI：
10.1128/iai.00311-06
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发表时间：
2006-10-01
影响因子：
3.1
通讯作者：
Kaufmann, Stefan H. E.
中科院分区：
文献类型：
--
作者：
Emoto, Masashi;Yoshizawa, Izumi;Kaufmann, Stefan H. E.
研究了细菌感染早期小鼠肝脏中CD 1d（糖脂/CD 1d）特异性V α 14（+）T细胞呈递糖脂的表型和功能变化。在单核细胞增生李斯特菌感染或白细胞介素-12（IL-12）治疗后，在正常胸腺和胸腺切除动物中，α-半乳糖神经酰胺/CD 1d四聚体反应性（α-GalCer/CD 1d（+））T细胞共表达自然杀伤（NK）1.1标志物变得不可检测，同时出现缺乏NK 1.1的细胞。NK1.1（+）亚群的消耗阻止了α-GalCer/CD 1d（+）NK1.1（-）T细胞的出现。在感染前，NK1.1（+），而不是NK1.1（-），共表达CD 4的α-GalCer/CD 1d（+）T细胞负责IL-4的产生，而γ干扰素（IFN-γ）由细胞产生，而不管NK1.1或CD 4的表达。感染后，在α-GalCer/CD 1d（+）T细胞中检测不到IL-4分泌细胞，但在NK1.1-细胞中发现了相当数量的IFN-γ分泌细胞，但在缺乏CD 4的NK1.1（+）细胞中没有。因此，V α 14（+）T细胞的NK1.1表面表达和功能活性在李斯特菌病的早期阶段经历了巨大的变化，并且这些变化以不依赖于胸腺的方式进展。在缺乏所有α-GalCer/CD 1d（+）T细胞的突变小鼠中，骨髓增生得到改善，表明NK1.1-T细胞亚群对抗菌保护的微妙贡献被NK1.1（+）T细胞亚群更深刻的有害作用所掩盖。
The phenotypic and functional changes of glycolipid presented by CD1d(glycolipid/CD1d) specific V alpha 14(+) T cells in the liver of mice at early stages of bacterial infection were investigated. After Listeria monocytogenes infection or interleukin-12 (IL-12) treatment, alpha-galactosylceramide/CD1d tetramer-reactive (alpha-GalCer/CD1d(+)) T cells coexpressing natural killer (NK) 1.1 marker became undetectable and, concomitantly, cells lacking NK1.1 emerged in both euthymic and thymectomized animals. Depletion of the NK1.1(+) subpopulation prevented the emergence of alpha-GalCer/CD1d(+) NK1.1(-) T cells. Before infection, NK1.1(+), rather than NK1.1(-), alpha-GalCer/CD1d(+) T cells coexpressing CD4 were responsible for IL-4 production, whereas gamma interferon (IFN-gamma) was produced by cells regardless of NK1.1 or CD4 expression. After infection, IL-4-secreting cells became undetectable among alpha-GalCer/CD1d(+) T cells, but considerable numbers of IFN-gamma-secreting cells were found among NK1.1-, but not NK1.1(+), cells lacking CD4. Thus, NK1.1 surface expression and functional activities of V alpha 14(+) T cells underwent dramatic changes at early stages of listeriosis, and these alterations progressed in a thymus-independent manner. In mutant mice lacking all alpha-GalCer/CD1d(+) T cells listeriosis was ameliorated, suggesting that the subtle contribution of the NK1.1- T-cell subset to antibacterial protection is covered by more profound detrimental effects of the NK1.1(+) T-cell subset.