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Fig. 5 | Experimental Hematology & Oncology

Fig. 5

From: Caspase-8 contributes to an immuno-hot microenvironment by promoting phagocytosis via an ecto-calreticulin-dependent mechanism

Fig. 5

Casp-8 malfunction hampered ecto-CRT transition and induced antigen presentation in B16F10-bearing mice. a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enriched in genes between Casp8 knockout and control B16F10 cells. Adjusted log10 p-values for the enrichment of KEGG gene sets are presented in color. b Heatmap of enriched genes in the lists of Antigen Processing and Presentation genes. c CD103+MHC-II+ dendritic cells in CD11c+ cells from drained lymph nodes in the subcutaneous mouse tumor model. d Statistical results of CD103+MHC-II+ cells dendritic cells. e and f B16F10 cells pre-labeled with the Deep Red dye were treated with Z-IETD-FMK and doxorubicin for 24 h. Labeled tumor cells were injected into the spleens of naive mice. Spleens were collected 2 h after mice received an intrasplenic injection. Splenocytes were subjected to immunostaining with a CD11c antibody to assess phagocytosis. Representative dot plots of flow cytometric analyses depicting the effect of the Casp8 inhibitor Z-IETD-FMK (e) and Casp8 knockout (f) are shown. Cell surface calreticulin expression (ecto-calreticulin) and total calreticulin in Z-IETD-FMK-treated (g) and Casp8 knockout (h) B16F10 cells

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