Fig. 7
From: RIP1 inhibition blocks inflammatory diseases but not tumor growth or metastases
Inactivation of RIP1 reduces arthritis and skin inflammation. a Sections of synovium from patients with rheumatoid arthritis (RA) and control human joints were immunolabeled with pRIP1 antibody; representative images are shown. Bars = 100 µm. Out of 20 examined RA samples, moderate to extensive labeling for pRIP1 was observed in 7/20 samples, rare to mild labeling in 8/20 samples and no labeling in 5/20 samples. Labeling for pRIP1 was also observed in 1/7 (moderate) and in 5/7 (rare to mild) normal samples. b Wild-type (WT) or Ripk1D138N/D138N (RIP1 KI) mice (n = 6 per group) were injected with 2 mg of a cocktail of anti-collagen antibodies on day 0 and monitored for 10 days. The scoring is a composite of all four paw scores. c Wild-type mice were treated as in b. On days 4–9 animals (n = 7 per group) were administered with vehicle and anti-ragweed-IgG2a (150 μg; cont), vehicle and mTNFR2-IgG2a (150 μg; TNFR2), GNE684 (50 mg/kg, PO, BID; 684) and anti-ragweed-IgG2a (150 μg; cont), or GNE684 and mTNFR2-IgG2a, and scored as in b. Asterisks indicate p < 0.05. d Histology of representative forepaws from c. Bars = 500 µm. e Sections of psoriatic and normal human skin were stained with pRIP1 antibody; representative images are shown. Bars = 50 µm. Immunolabeling for pRIP1 was observed in 4 out of 20 psoriasis samples, and in none of four normal samples. f Wild-type or Sharpin mutant (Cpdm) mice treated with vehicle (n = 9 for WT and n = 7 for Cpdm) or GNE684 (50 mg/kg, PO, BID, n = 7; 684) for 4.5 days. Dorsal and ventral cervical skin tissues were scored separately and added for the total skin histologic score
