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Characterization of lung infection–induced TCRγδ T cell phenotypes by CyTOF mass cytometry

生物 流式细胞术 T细胞 白细胞介素2受体 质量细胞仪 分化群 T细胞受体 分子生物学 受体 细胞毒性T细胞 免疫系统 细胞 免疫学 细胞生物学 表型 体外 生物化学 遗传学 基因
作者
Lorenz Wanke-Jellinek,Joshua Keegan,James W. Dolan,James A. Lederer
出处
期刊:Journal of Leukocyte Biology [Wiley]
卷期号:99 (3): 483-493 被引量:18
标识
DOI:10.1189/jlb.4a0315-115rr
摘要

Abstract T cell receptor γδ cells are known to be the primary effector T cells involved in the response to bacterial infections, yet their phenotypic characteristics are not as well established as other T cell subsets. In this study, we used cytometry by time-of-flight mass cytometry to better characterize the phenotypic response of T cell receptor γδ cells to Streptococcus pneumoniae lung infection. Mice were infected, and cells from lung washouts, spleen, and lymph nodes were stained to detect cell-surface, intracellular, and signaling markers. We observed that infection caused a significant increase in T cell receptor γδ cells, which expressed high interferon-γ and interleukin-17A levels. Profiling T cell receptor γδ cells by cytometry by time-of-flight revealed that activated γδ T cells uniquely coexpressed cell-surface Gr-1, cluster of differentiation 14, and cluster of differentiation 274 (programmed death-ligand 1). Further classification of Gr-1 expression patterns on T cell receptor γδ cells demonstrated that Gr-1+ T cell receptor γδ cells were the primary source of interferon-γ, whereas Gr-1− cells mostly expressed interleukin-17A. Gr-1+ T cell receptor γδ cells also showed higher ζ-chain–associated protein kinase 70, p38, and 4eBP1 signaling in response to infection as compared with Gr-1− T cell receptor γδ cells. Taken together, Gr-1 expression patterns on γδ T cells in the lung provide a robust marker to differentiate interferon-γ– and interleukin-17A–producing subsets involved in the early immune response to bacterial pneumonia.
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