摘要：SummaryTo assess the cross-talk between immune cells and respiratory tract during SARS-CoV-2 infection, we analyzed the relationships between the inflammatory response induced by SARS-CoV-2 replication and immune cells phenotype in a reconstituted organotypic human airway epithelium (HAE). The results indicated that immune cells failed to inhibit SARS-CoV-2 replication in the HAE model. In contrast, immune cells strongly affected the inflammatory profile induced by SARS-CoV-2 infection, dampening the production of several immunoregulatory/inflammatory signals (e.g., IL-35, IL-27, and IL-34). Moreover, these mediators were found inversely correlated with innate immune cell frequency (NK and γδ T cells) and directly with CD8 T cells. The enriched signals associated with NK and CD8 T cells highlighted the modulation of pathways induced by SARS-CoV-2 infected HAE. These findings are useful to depict the cell-cell communication mechanisms necessary to develop novel therapeutic strategies aimed to promote an effective immune response.Graphical abstractDisplay OmittedHighlights•HAE as a model to study the cross-talk between infected epithelium and immune cells•Immune cells failed to inhibit SARS-CoV-2 replication•Immune cells dampen the production of several signals induced by SARS-CoV-2 infection•Decrease of NK/γδ T and increase of CD8 T cells in SARS-CoV-2 infected HAE co-cultureImmunology; Virology
