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Aurora A controls CD8(+) T cell cytotoxic activity and antiviral response

Aurora 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 whet...

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Detalles Bibliográficos
Autores principales: Bustos-Morán, Eugenio, Blas-Rus, Noelia, Alcaraz-Serna, Ana, Iborra, Salvador, González-Martínez, José, Malumbres, Marcos, Sánchez-Madrid, Francisco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379542/
https://www.ncbi.nlm.nih.gov/pubmed/30778113
http://dx.doi.org/10.1038/s41598-019-38647-y
Descripción
Sumario:Aurora 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.