Supplementary Material for: The Antimicrobial Peptide hLF1–11 Drives Monocyte-Dendritic Cell Differentiation toward Dendritic Cells That Promote Antifungal Responses and Enhance Th17 Polarization

The hLF1–11 peptide comprising the first 11 N-terminal residues of human lactoferrin exerts antimicrobial activity in vivo, enhances the inflammatory response of monocytes and directs monocyte-macrophage differentiation toward cells with enhanced antimicrobial properties. In this study, we investigated the effects of hLF1–11 on human monocyte-dendritic cell (DC) differentiation and subsequent T cell activation. Results revealed that – compared to control (peptide-incubated) DCs – hLF1–11-differentiated DCs displayed enhanced expression of HLA class II antigens and dectin-1, and increased phagocytosis of <i>Candida albicans</i>. In addition, hLF1–11-differentiated DCs produced enhanced amounts of reactive oxygen species, IL-6 and IL-10, but not IL-12p40 and TNF-α, upon stimulation with <i>C. albicans</i>. Moreover, 6-day-cultured hLF1–11-differentiated DCs and control (peptide-incubated) DCs that had been stimulated with a Th17-inducing mix of antigens (including <i>C. albicans</i>) for 24 h were cocultured with autologous CD4+ T cells for 72 h and then the levels of IL-10, IL-17 and IFN-γ production and the percentage of cytokine-producing T cells were assessed. The results revealed that the hLF1–11-differentiated DCs induced an enhanced IL-17, but reduced IFN-γ, production by T cells as compared to control (peptide-incubated) DCs. Collectively, the hLF1–11 peptide drives monocyte-DC differentiation toward DCs that promote antifungal responses and enhance Th17 polarization.