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. 2016 May 20;7(25):38451–38466. doi: 10.18632/oncotarget.9498

Figure 6. Nicotine-increased cross-presentation requires the endosomal recruitment of TAP via IRAK4 signaling.

Figure 6

Nicotine-treated IRAK4 deficient and control DCs were incubated with endotoxin-free OVA with short term exposure of LPS. A. Flow cytometric determination of cross-presented OVA in DCs. Numbers in histogram indicates MFI of analyzed population. B. BrdU cell proliferation assay of splenocytes co-cultured with OVA-pulsed DCs. C. ELISA of IL-12 in supernatants of splenocytes co-cultured with OVA-pulsed DCs. IFN-γ Elispot assay of OVA-specific CD8+ T cells in the splenocytes D. and lymph nodes E. of the recipients which conferred intraperitoneal DCs transfer. F. Immunofluorescence observation of the recruitment of TAP toward endodomes. TAP (green); Rab5, EEA1, Rab7 (all red); nuclei are counterstained with DAPI (blue). Original magnification, ×600. G. Immunofluorescence observation of IRAK4 deficiency on nicotine-increased cross-presentation. Cross-presented OVA is stained with 25-D1.16 (red); MHC class I (green); EEA1 in 25-D1.16 co-localization is green and in MHC class I co-localization is red; nuclei are counterstained with DAPI (blue). Original magnification, ×600. The data are presented as the mean±SEM, *p<0.05, **p<0.01, ***p<0.001, one-way ANOVA with Newman-Keulspost test. One representative from 3 independent experiments is shown. Ni: nicotine; si: siRNA.