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. Author manuscript; available in PMC: 2018 Feb 13.
Published in final edited form as: Cancer Cell. 2017 Feb 13;31(2):194–207. doi: 10.1016/j.ccell.2017.01.004

Figure 8. Pharmacologic stabilization of IFNAR1 disrupts immune privileged niche and elicits a therapeutic effect against tumors.

Figure 8

(A) Immunoblot analysis of phosphorylation and levels of p38α and PKD2 kinases in cultured MC38 cells and MC38 tumors.

(B) Levels of cell surface IFNAR1 on tumor infiltrating CD3+CD8+ cells isolated from MC38 tumors grown in WT or Ifnar1-null mice treated with kinase inhibitors as indicated. Representative FACS and quantification are shown.

(C) Frequency of CD8+ T cells (% of CD45+ cells) isolated from MC38 tumors grown in WT or Ifnar1-null mice treated with kinase inhibitors as indicated.

(D) Quantification of results shown in panel C.

(E) Anti-tumor effect of SD-208 and LY2228820 administered to Ifnar1−/− and WT mice bearing MC38 tumors as described in Methods.

Data are shown as Mean±SEM (n=5 from each of 3 independent experiments).

See also Figure S8