Bustos-Morán, EugenioBlas-Rus, NoeliaAlcaraz-Serna, AnaIborra, SalvadorGonzález-Martínez, JoséMalumbres Martinez, MarcosSanchez-Madrid, Francisco2019-02-212019-02-212019-02-18Sci Rep. 2019; 9(1):22112045-2322http://hdl.handle.net/20.500.12105/7212Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4+ T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8+ T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8+ T cells. This finding was similarly proven for both mice and human CD8+ CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as granzyme B or perforin1. Finally, we have found that Aurora A is necessary for CD8+ T cell-mediated antiviral response, in an in vivo model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.engVoRhttp://creativecommons.org/licenses/by/4.0/Atribución 4.0 Internacional3077811391221110.1038/s41598-019-38647-y2045-2322Scientific reportsopen access