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. 2024 Feb 29;18(10):7618–7632. doi: 10.1021/acsnano.4c00550

Figure 5.

Figure 5

Understanding the mechanism behind DC activation by AnCHNPs. (a) A heatmap showing the top 10 most upregulated genes in AnCHNPs-treated BMDCs (vs Ctrl) (n = 3). (b) GO enrichment analysis of the top 10 GO terms resulting from upregulated DGEs in AnCHNPs-treated BMDCs (vs Ctrl). (c) GSEA analysis of enrichment plots for a priori gene sets for the top 4 most upregulated pathways in AnCHNPs-treated BMDCs (vs Ctrl). GSEA, gene set enrichment analysis; NES, normalized enrichment score. (d) Expression of selected cytokine and chemokine genes by RT-qPCR (n = 3). Data are presented as the mean ± s.d. *, p < 0.05; **, p < 0.01; ***, p < 0.001. (e) Western blot examining proteins of interest. BMDCs were treated with OVA (10 μg/mL) (Ctrl) or OVA (10 μg/mL) plus AnCHNPs (5 μg/mL) for 24 h. (f) Schematic illustration of the activation mechanism. The endocytosis of AnCHNPs is followed by particle degradation in the lysosome and Ca2+ release into the cytosol. The increase in [Ca2+]int leads to the activation of the NF-κB and NFAT pathways, eliciting antigen-presenting molecules, costimulatory molecules, and pro-inflammatory cytokines.