Skip to main content
. 2018 Aug 6;14(8):e1007234. doi: 10.1371/journal.ppat.1007234

Fig 4. Type I IFNs induce caspase-independent HSPC death during IOE infection.

Fig 4

(A) Fold change in dead/dying cell frequency within the CD48- HSPC population of WT and Ifnar1-/- mice 7 d.p.i. normalized to WT mock levels. n = 5–9 mice/group. (B) Fold change in the proportion of live HSPCs with active caspases 8 or 3/7 over mock mice. n = 3–6 mice/group. (C) Frequency of apoptotic (Annexin V+ 7AAD-), dying (Annexin V+ 7AAD+), and dead (Annexin V- 7AAD+) cells and (D) caspase 8 or 3/7-active cells (gated on live, 7AAD- cells) among WT and Ifnar1-/- HSPCs in mixed BM chimeric mice 7 d.p.i. n = 3 mice. (E) Detection of full length RIP1, cleaved RIP1, full length RIP3, cleaved RIP3, and actin in BM lysates of WT and Ifnar1-/- mock and IOE–infected mice 7 d.p.i. Lanes represent individual mice. (F) Fold change of cleaved RIP1 to full length RIP1 and cleaved RIP3 to full length RIP3 in WT and Ifnar1-/- mock (m) and IOE–infected mice, 7 d.p.i. *P < 0.05, **P < 0.001, ***P < 0.0001.