Ablation of CD103+ cDC1s in Langerin-DTR and Batf3−/− transgenic mice has been shown to significantly diminish the virus-specific CTL population in models of mouse infection (1, 6), although the specific mechanisms regulating virus-specific CTL numbers in the respiratory tract, as well as the development of memory CD8+ T cell responses, have not been fully elucidated. Here, ITGAE is linked to infection.