For example, AMs promote BRM cells to migrate into secondary influenza-infected sites to enhance anti-virus immunity.131 Moreover, IL-18 produced by AMs contributes to the establishment of CD103+CD8+TRM cells and the expansion of CD8+TRM cells upon influenza reinfection.482 Conclusively, the development of vaccines that can induce TRM and BRM cells to amplify host defense against virus infection is a promising strategy. This evidence concerns the gene ITGAE and influenza.