生物
巨噬细胞
脂多糖
免疫学
脾脏
免疫系统
淋巴细胞
促炎细胞因子
微生物学
体外
炎症
生物化学
作者
Rui Ding,Haoran Xu,Han Hsiang Huang,Ruibing Cao,Yingjun Lv
出处
期刊:Viral Immunology
[Mary Ann Liebert, Inc.]
日期:2024-04-01
卷期号:37 (3): 139-148
被引量:3
标识
DOI:10.1089/vim.2023.0098
摘要
with GAstV-2, and the virus localization in the lymphocytes and macrophages, proliferation and apoptosis of lymphocytes, and phagocytic activity, reactive oxygen species (ROS) and nitric oxide (NO) production, and cell polarity in macrophages were determined. The results showed that GAstV-2 was observed in the cytoplasm of CD4 and CD8 T cells and macrophages, indicating that GAstV-2 can infect both lymphocytes and macrophages. GAstV-2 infection reduced the lymphocyte proliferation induced by Concanavalin A and lipopolysaccharide stimulation and increased the lymphocyte apoptosis rate and mRNA expression of Fas, demonstrating that GAstV-2 causes damage to lymphocytes. Moreover, GAstV-2 infection enhanced phagocytic activity and production of ROS and NO and induced a proinflammatory phenotype in macrophages (M1 macrophages), indicating that macrophages play an antiviral role during GAstV-2 infection. In conclusion, these results demonstrate that GAstV-2 infection causes damages to lymphocytes, and host macrophages inhibit GAstV-2 invasion during infection.
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