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Fig. 4 | BMC Immunology

Fig. 4

From: PU.1-CD23 signaling mediates pulmonary innate immunity against Aspergillus fumigatus infection by driving inflammatory response

Fig. 4

PU.1 directly activated the expression of CD23 in HTMs with AF infection. A Luciferase reporter plasmid containing two putative PU.1 binding sites in the CD23 promoter (2500 bp upstream of the ATG) compared to the full-length promoter deletion (300 bp upstream of the ATG). B Dual luciferase reporter assay showed that PU.1 could activate the LUC signal in the construct containing sequences from 2500 bp upstream of the ATG to 50 bp downstream of ATP. The luciferase activities were normalized to the β-galactosidase levels of the control. C Three artificial mutations in the PU.1 binding sites of the CD23 promoter. D Relative LUC activity showed the activating efficiency of PU.1 to the three artificial mutated CD23 promoters. E CD23 promoter revealed two putative PU.1 binding sites starting at -695 and -326. F Relative DNA levels of the CD23 promoter region containing two PU.1 binding sites from ChIP assay were detected by qPCR. G Percentage relative to input DNA for PU.1 ChIP was quantified. H EMSA showed that the PU.1 protein could bind to the CD23 promoter region in vitro. All data are presented as the mean ± SD, N ≥ 3, *P < 0.05, **P < 0.01

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