Laboratory of Pathology and Immunology of Aquatic Animals, KLMME, Ocean University of China, Qingdao, China.
Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China.
Front Immunol. 2019 Jul 16;10:1622. doi: 10.3389/fimmu.2019.01622. eCollection 2019.
B cells have recently been proven to have phagocytic activities, but few studies have explored the relevant regulation mechanisms. In this study, we showed that the Japanese flounder () membrane-bound (m)IgM B lymphocyte population could phagocytose inactivated with a mean phagocytic rate of 25%. High-purity mIgM B lymphocytes were subsequently sorted to investigate the cellular response to stimulation . Transcriptome analysis identified 1,375 differentially expressed genes (DEGs) after stimulation, including 975 upregulated and 400 downregulated genes. Many of these DEGs were enriched in multiple pathways associated with phagocytosis such as focal adhesion, the phagosome, and actin cytoskeleton regulation. Moreover, many genes involved in phagolysosomal function and antigen presentation were also upregulated after stimulation, indicating that mIgM B lymphocytes may degrade the internalized bacteria and present processed antigenic peptides to other immune cells. Interestingly, the type I interferon 3 ( gene was upregulated after stimulation, and further analysis showed that the recombinant (r)IFN I-3 significantly enhanced phagocytosis of and by mIgM B lymphocytes. In addition, significantly higher intracellular reactive oxygen species (ROS) levels were detected in mIgM B lymphocytes following rIFN I-3 treatment. We also found that IFN I-3 significantly upregulated expression in mIgM B lymphocytes, and the enhancing effect of IFN I-3 on mIgM B lymphocyte-mediated phagocytosis was suppressed by fludarabine treatment. Collectively, these results demonstrate that mIgM B cell-mediated phagocytosis in the Japanese flounder is effectively triggered by bacterial stimulation, and further enhanced by IFN I-3, which itself may be regulated by Stat1.
B 细胞最近被证明具有吞噬活性，但很少有研究探讨相关的调节机制。在这项研究中，我们表明，牙鲆（）膜结合（m）IgM B 淋巴细胞群体可以吞噬失活的，平均吞噬率为 25%。随后，我们分选高纯度的 mIgM B 淋巴细胞，以研究细胞对刺激的反应。转录组分析鉴定出刺激后 1375 个差异表达基因（DEGs），包括 975 个上调基因和 400 个下调基因。这些 DEGs 中的许多基因富集在与吞噬作用相关的多个途径中，如焦点黏附、吞噬体和肌动蛋白细胞骨架调节。此外，许多参与吞噬溶酶体功能和抗原呈递的基因在刺激后也上调，表明 mIgM B 淋巴细胞可能降解内化的细菌并将加工的抗原肽呈递给其他免疫细胞。有趣的是，刺激后 I 型干扰素 3（基因上调，进一步分析表明，重组（r）IFN I-3 显著增强了 mIgM B 淋巴细胞对和的吞噬作用。此外，在 rIFN I-3 处理后，mIgM B 淋巴细胞中检测到明显更高的细胞内活性氧（ROS）水平。我们还发现，IFN I-3 显著上调 mIgM B 淋巴细胞中的表达，而 IFN I-3 对 mIgM B 淋巴细胞介导的吞噬作用的增强作用被氟达拉滨处理所抑制。总之，这些结果表明，牙鲆 mIgM B 细胞介导的吞噬作用被细菌刺激有效触发，并进一步被 IFN I-3 增强，而 IFN I-3 本身可能受到 Stat1 的调节。
