Early Transient IFN-γ Production-dependent and Independent Mechanisms Underlie the Cross-protectivity of Lung-Resident Memory CD8 T Cells against Respiratory Virus Challenge

Transcriptome profiling of lung tissues and lung CD8+ TRM during early phase of infection to investigate the mechanism of lung TRM cells during antigen re-exposure within 48hours. After P14 T cell transfer, PR8 infection would not induce P14 TRM cells, while PR8-gp33 would. Comparing the gene expression of lung tissues after LCMV Armstrong challenge at day 30 after PR8 or PR8-gp33 infection would help us understand the function of lung CD8+ TRM cells. Sorted TRM cells from mice challenged with LCMV Armstrong at day 30 after PR8-gp33 infection would reveal the activation mechanism of TRM cells. TCR-transgenic P14 T cells were adoptively transferred to generate immune chimeras. At various time points post LCMV Armstrong infection, P14 Trm cells were sorted from lung BAL based on their surface expression of CD45.1+CD69+CD11a-, and microarray was performed. RNA of lung tissue from sequential infection of PR8 and Armstrong and of PR8-gp33 and Armstrong was extracted and sent for microarray analysis.