Journal article

Nociceptive sensory neurons promote CD8 T cell responses to HSV-1 infection

Jessica Filtjens, Anais Roger, Linda Quatrini, Elisabeth Wieduwild, Jordi Gouilly, Guillaume Hoeffel, Rafaelle Rossignol, Clara Daher, Guilhaume Debroas, Sandrine Henri, Claerwen M Jones, Bernard Malissen, Laura K Mackay, Aziz Moqrich, Francis R Carbone, Sophie Ugolini

NATURE COMMUNICATIONS | NATURE RESEARCH | Published : 2021

Abstract

Host protection against cutaneous herpes simplex virus 1 (HSV-1) infection relies on the induction of a robust adaptive immune response. Here, we show that Nav1.8+ sensory neurons, which are involved in pain perception, control the magnitude of CD8 T cell priming and expansion in HSV-1-infected mice. The ablation of Nav1.8-expressing sensory neurons is associated with extensive skin lesions characterized by enhanced inflammatory cytokine and chemokine production. Mechanistically, Nav1.8+ sensory neurons are required for the downregulation of neutrophil infiltration in the skin after viral clearance to limit the severity of tissue damage and restore skin homeostasis, as well as for eliciting ..

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Grants

Awarded by European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme


Awarded by Agence Nationale de la Recherche (ANR)


Funding Acknowledgements

We thank Justine Galluso for mouse breeding and genotyping. We thank Melanie Gabriac for the preliminary work performed during the initial phase of this project. We thank the Centre d'Immunologie de Marseille-Luminy (CIML) mouse house and core cytometry facilities. This project received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme, under grant agreement No. 648768, from the Agence Nationale de la Recherche (ANR) (No. ANR-14-CE14-00 09-01), and the Fondation pour la Recherche Medicale (FRM). This work was also supported by institutional grants from INSERM, CNRS, Aix-Marseille University and Marseille-Immunopole to the CIML.