Fig. 4: TNFR1 ablation rescues Ripk1K376R/K376R embryonic lethality but not tissue inflammation.
From: Impaired RIPK1 ubiquitination sensitizes mice to TNF toxicity and inflammatory cell death
a Numbers of offspring at E12.5 and perinatal day 1 (P1) from intercrossing Tnfr1−/− Ripk1K376R/+ mice. b Representative image of Tnfr1−/− Ripk1+/+ and Tnfr1−/− Ripk1K376R/K376R pups at P7. c Representative embryos of the Tnfr1−/− Ripk1K376R/+ intercross. Scale bars on the top left of each image indicate 2 mm. d Yolk sac of Tnfr1−/− Ripk1+/+ and Tnfr1−/− Ripk1K376R/K376R intercross immunolabeled for with cleaved caspase-3 [green] and PECAM-1 [red] [scale bar 50 μm]. e IHC for cleaved caspase-3 of the representative embryos at E12.5. [scale bar 200 μm]. f Representative histology of skin [scale bar 200 μm] and liver [scale bar 50 μm] of Tnfr1−/− Ripk1+/+ and Tnfr1−/− Ripk1K376R/K376R. g Serum level cytokines and chemokines of MIP-1β, MCP-1, RANTES and IL-6 of Tnfr1−/− Ripk1K376R/K376R pups [n = 6] and littermate controls [n = 5]. Mean values with SD is plotted [N.D. not detected, 2 littermate control samples did not show detectable concentrations for IL-6]. h Lung of adult Ripk1K376R/K376R Casp8−/− Ripk3−/− mice showed increased perivascular and peribronchiolar lymphoid aggregates compared to Ripk1+/+ Casp8−/− Ripk3−/− mice [scale bar 100 μm].
