The roles of osteopontin and IL-17 in the protective immune responses against virus infection

在本研究中，我们发现甲型流感病毒感染后，肺和淋巴组织（如脾脏）均诱导了Opn的表达。尽管初始免疫反应在开放蛋白缺陷小鼠和开放蛋白完整小鼠之间是相似的，但在感染后60天，开放蛋白缺陷小鼠保持了更多的病毒特异性记忆CD8^+T细胞。到目前为止，我们假设骨桥蛋白通过通过抗原呈递细胞调节IL-12的产生来调节甲型流感病毒感染后记忆性CD8^+T细胞的产生。

In this study, we found that Opn expression is induced both in the lung and lymphoid tissues such as spleen following influenza A virus infection. Although initial immune responses are comparable between Opn-deficient and Opn-intact mice, Opn-deficient mice maintained more virus-specific memory CD8^+T cells at 60 days after infection. So far, we assume that osteopontin modulates the generation of memory CD8^+T cells following influenza A virus infection through presumably regulating IL-12 production by antigen presenting cells.