Fig. 2

Host response to oral pathogen influx. A protective host response to infection is dependent on dendritic cell-mediated induction of Th17 cell-mediated adaptive immunity, which, by the production of interleukin (IL)-17 upregulates the innate expression of mucosal antimicrobial peptides (β-defensins, calprotectin) by epithelial cells. IL17 also up-regulates IL8 and granulocyte–macrophage colony-stimulating factor (GM-CSF) production by epithelial cells, which in turn trigger recruitment of polymorphonuclear neutrophils (PMN) to the oral mucosa. Innate-like cell populations, including γδ T-cells, Natural Killer T cells (NKT), innate lymphoid cells (ILC) and natural Th17 cells (nTh17), also produce IL17 and may participate in the mucosal host response. CLRs, C-type lectin receptors; RNIs, reactive nitrogen intermediates; ROIs, reactive oxygen intermediates; and TLRs, toll-like receptors. Image adapted from (Repentigny et al. 2015) under the Creative Commons Attributions License 4.0 International (CC BY 4.0)