World journal of emergency medicine · 2022
Neutrophils inhibit CD8+ T cells immune response by arginase-1 signaling in patients with sepsis.
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Dai Xiao-Kang, Ding Zhen-Xing, Tan Yuan-Yuan, Bao Hua-Rui, Wang Dong-Yao, Zhang Hong
Аннотация
BACKGROUND: Patients with sepsis often exhibit an acute inflammatory response, followed by an immunosuppressive phase with a poor immune response. However, the underlying mechanisms have not been fully elucidated.
METHODS: We sought to comprehensively characterize the transcriptional changes in neutrophils of patients with sepsis by transcriptome sequencing. Additionally, we conducted a series of experiments, including real-time quantitative polymerase chain reaction (RT-qPCR) and flow cytometry to investigate the role of arginase-1 signaling in sepsis.
RESULTS: Through the analysis of gene expression profiles, we identified that the negative regulation of T cell activation signaling was enriched, and the expression of arginase-1 was high in neutrophils from patients with sepsis. Furthermore, we conducted flow cytometry and found that the function of CD8+ T cells in septic patients was impaired. Moreover, neutrophils from septic patients inhibited the percentage of polyfunctional effector CD8+ T cells through arginase-1. Additionally, the proportions of granzyme B+IFN-γ+CD8+ T and TNF-α+IFN-γ+CD8+ T cells increased after inhibition of arginase-1 signaling.
CONCLUSION: The impaired effector function of CD8+ T cells could be restored by blocking arginase-1 signaling in patients with sepsis.
METHODS: We sought to comprehensively characterize the transcriptional changes in neutrophils of patients with sepsis by transcriptome sequencing. Additionally, we conducted a series of experiments, including real-time quantitative polymerase chain reaction (RT-qPCR) and flow cytometry to investigate the role of arginase-1 signaling in sepsis.
RESULTS: Through the analysis of gene expression profiles, we identified that the negative regulation of T cell activation signaling was enriched, and the expression of arginase-1 was high in neutrophils from patients with sepsis. Furthermore, we conducted flow cytometry and found that the function of CD8+ T cells in septic patients was impaired. Moreover, neutrophils from septic patients inhibited the percentage of polyfunctional effector CD8+ T cells through arginase-1. Additionally, the proportions of granzyme B+IFN-γ+CD8+ T and TNF-α+IFN-γ+CD8+ T cells increased after inhibition of arginase-1 signaling.
CONCLUSION: The impaired effector function of CD8+ T cells could be restored by blocking arginase-1 signaling in patients with sepsis.