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. Author manuscript; available in PMC: 2019 May 3.
Published in final edited form as: Cell. 2018 Mar 22;173(4):920–933.e13. doi: 10.1016/j.cell.2018.02.055

Figure 3. IRF8 is a key factor in transcriptional regulation of NAIPs.

Figure 3

(A) Microarray analysis of the expression of pattern recognition receptor (PRR)–encoding genes 4 h after infection with S. Typhimurium (MOI, 0.1) in Irf8−/− BMDMs relative to that of WT.

(B) Interaction network visualizing the associations between IRF8, IRF4, SPI1, NLRC4, and NAIPs.

(C) Chromatin immunoprecipitation-sequencing (ChIP-seq) for IRF8 binding in Naip1, Naip2, Naip5, Naip6, and Nlrc4. Peaks indicate regions of DNA bound by IRF8.

(D) Real-time (RT)-PCR analysis of genes encoding NAIPs in BMDMs before (0 h) and after (1 h or 3 h) infection with S. Typhimurium, presented relative to levels of the gene encoding HPRT.

(E) RT-PCR analysis of genes encoding NAIP5 and NAIP6 in BMDMs before (0 h) and after (1 h or 3 h) transfection with 0.5 μg flagellin, presented relative to levels of the gene encoding HPRT.

(F) RT-PCR analysis of genes encoding NLRP3 and NLRC4 in untreated BMDMs, presented relative to levels of the gene encoding HPRT.

(G) ChIP-seq for IRF4 binding in Naip2 and Naip5.

(H) ChIP-seq for SPI1 binding in Naip1, Naip2, Naip5, and Naip6, shown as MACS2 called peaks.

NS, not significant; and **P < 0.01 (two-tailed t test). Data (D–F) are from 3 independent experiments (mean ± SEM).