Chemokines cooperate with TNF to provide protective anti-viral immunity and to enhance inflammation

Alí Alejo, M. Begoña Ruiz-Argüello, Sergio M. Pontejo, María del Mar Fernández de Marco, Margarida Saraiva, Bruno Hernáez and Antonio Alcamí ()
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Alí Alejo: Centro de Investigación en Sanidad Animal; Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Valdeolmos
M. Begoña Ruiz-Argüello: Centro de Investigación en Sanidad Animal; Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Valdeolmos
Sergio M. Pontejo: Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid), Cantoblanco
María del Mar Fernández de Marco: Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid), Cantoblanco
Margarida Saraiva: University of Cambridge, Addenbrooke’s Hospital
Bruno Hernáez: Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid), Cantoblanco
Antonio Alcamí: Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid), Cantoblanco

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract The role of cytokines and chemokines in anti-viral defense has been demonstrated, but their relative contribution to protective anti-viral responses in vivo is not fully understood. Cytokine response modifier D (CrmD) is a secreted receptor for TNF and lymphotoxin containing the smallpox virus-encoded chemokine receptor (SECRET) domain and is expressed by ectromelia virus, the causative agent of the smallpox-like disease mousepox. Here we show that CrmD is an essential virulence factor that controls natural killer cell activation and allows progression of fatal mousepox, and demonstrate that both SECRET and TNF binding domains are required for full CrmD activity. Vaccination with recombinant CrmD protects animals from lethal mousepox. These results indicate that a specific set of chemokines enhance the inflammatory and protective anti-viral responses mediated by TNF and lymphotoxin, and illustrate how viruses optimize anti-TNF strategies with the addition of a chemokine binding domain as soluble decoy receptors.

Date: 2018
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DOI: 10.1038/s41467-018-04098-8

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