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. Author manuscript; available in PMC: 2020 Jun 9.
Published in final edited form as: Nat Immunol. 2019 Dec 9;21(1):54–64. doi: 10.1038/s41590-019-0550-7

Figure 2. Caspase-8 and Ripk3/Mlkl drives footpad inflammation in Ptpn6 mutant mice.

Figure 2.

a) Immunoblot for cleaved caspase-8 and Ptpn6 from freshly-isolated wild-type and Ptpn6ΔPMN bone marrow neutrophils. Luminescence was quantified using a ChemiDoc Gel Imaging System and ImageLab software. Mean ± SEM, n=4 independent neutrophil samples from Ptpn6ΔPMN or wild-type littermate controls. Data analyzed by Student’s t test. p values are shown. b) Kaplan-Meier plots showing disease-free survival of Ptpn6ΔPMN mice (n=145) compared with Ptpn6ΔPMNRipk3−/− (n=15), Ptpn6ΔPMNRipk3−/−caspase-8ΔPMN (n=45) mice, Ptpn6ΔPMNMlkl−/− (n=10), Ptpn6ΔPMNcaspase-8ΔPMNMlkl−/− (n=35) mice, Ptpn6ΔPMNcaspase-8ΔPMN (n=49), Ptpn6ΔPMNcaspase-8ΔPMNRipk3−/−Mlkl−/− (n=34), Ptpn6ΔPMNRipk1ΔPMN (n=9) and Ptpn6ΔPMNRipk1ΔPMN/D138N (n=8) mice. Survival curves were analyzed using a log-rank (Mantel-Cox) test compared to Ptpn6ΔPMN mice. Each panel shares the disease-free survival data of Ptpn6ΔPMN mice. c) RNA-Seq transcriptomic analysis of bone marrow neutrophils from female Ptpn6ΔPMN mice lacking Ripk3, Mlkl, and/or Casp8. Values are gene-wise z-scores of counts using the variance stabilized transformation from DESeq2.