The Dendritic Cell Strikes Back In Coxsackievirus A10 Infection

Abstract

Abstract Coxsackievirus A10 (CV-A10) is a major causative pathogen of hand, foot, and mouth diseases (HFMDs). Currently, there is no effective vaccine for CV-A10. Dendritic cells (DCs) support antiviral immunity by linking innate and adaptive immune responses. DCs stimulated with different kinds of antigens have been used in recent vaccine studies for cancer with promising results so far. Here we examined DC dynamics during CV-A10 infection to uncover how they exert their functions and elucidate the significance and value of assessing the immunogenicity and immunoprotection of dendritic cell vaccination candidates on CV-A10-infected rhesus monkeys. We found that, dendritic cells expressing the surface marker CD11c showed an abnormal biological phenotype, including the altered transcription of various immune signaling molecules and inflammatory factors associated with innate immunity after viral replication. Furthermore, these CV-A10-infected dendritic cells have the capacity to stimulate the proliferation of T cells and to enhance the release of certain functional cytokines. An adaptive immune response induced by the back-transfusion of CV-A10-infected dendritic cells was observed in donor neonatal rhesus monkeys. Collectively, these data proposed that CV-A10 infection induced a strong innate immune response in rhesus monkey DCs, performing the function of the antigen-presenting response of this cell, which may provide helpful insights into the pathogenesis and vaccine research of CV-A10 in human.