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| The effect of suppressing PD-L1 expression of neutrophils on immunoactivity of T lymphocytes during sepsis |
| YU Yao1， SUN Hui1， LIU Yi-shu1, QI Xin-xin1， LIU Lu1， SUN Bing-wei2 |
| （1. School of Medicine, Jiangsu University, Zhenjiang Jiangsu 212013; 2. Department of Burns and Plastic Surgery, Suzhou Hospital Affiliated to Nanjing Medical University, Suzhou Jiangsu 215008, China) |
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Abstract Objective: To investigate the effect of neutrophils on T lymphocytes during sepsis and its potential mechanism. Methods: Sepsis model in vitro was established by co-culturing T lymphocytes with lipopolysaccharide(LPS). Neutrophils were isolated by density gradient centrifugation and T lymphocytes were isolated by anti-CD3 magnetic beads from human peripheral blood. T lymphocytes were divided into 4 groups, including control group, LPS group, neutrophil group and LPS+ neutrophil group. The apoptosis, proliferation, activation and secretion of T lymphocytes were assessed by flow cytometry. Phenotype programmed deathligand 1(PD-L1) on neutrophil was detected in control group and LPS group. Anti-PD-L1 antibody was added into mixed culture of neutrophils with T cells and the apoptosis of T cells were assessed. Results: Compared with the control group, neutrophil group and LPS + neutrophil group showed significantly lower immunoactivity of T lymphocytes, higher proportion of apoptosis, lower expression levels of CD69 and CD71, as well as secretion of interferon-γ(IFN-γ) and IL-2(all P<0.05). Compared with LPS group, the proliferation of T cells, secretion of IFN-γ and IL-2 were decreased in LPS+ neutrophilgroup (all P<0.05). The ratio of PD-L1 in LPS group was significantly higher than that of the control group (P<0.05). The proportion of viable lymphocytes increased with higher concentrations of PD-L1 monoclonal antibody (all P<0.05). Conclusion: Neutrophils suppressed the immunoactivity of T lymphocytes through PD-L1/PD-1 pathway during sepsis.
［Key words］sepsis; neutrophil; T lymphocyte; programmed death-ligand 1
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Received: 12 October 2018
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2018, Vol. 28 
