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. 2014 Nov 24;111(49):17582–17587. doi: 10.1073/pnas.1409700111

Fig. 4.

Fig. 4.

JNP facilitates Treg accumulation. (A) Foxp3 immunostains in liver parenchymas of 11-mo-old Mdr2−/−c-JunWT/WT or Mdr2−/−c-JunAA/AA mice. (Scale bars: 100 μm.) Insets show higher magnification of boxed regions. (B) Immunoquantification of Foxp3+ cells, shown in A, by analyzing multiple sections from each sample, representing the entire liver (n = 10, mean ± SEM). (C) qPCR analysis of Foxp3 expression in total liver lysates of 11-mo-old mice (n = 9; mean ± SEM). (D and E) Liposomal LPS-induced chronic inflammation. Results are representative of three experiments. (D) FACS analysis of percentage of CD4+Foxp3+ Treg cells in peripheral blood lymphocytes (PBLs) and spleens (n = 3; mean ± SEM). (E) Foxp3 mRNA levels in splenocytes (n = 3; mean ± SEM). (F and G) Treg cells were isolated from Mdr2−/−c-JunWT/WT mice, labeled with CFSE, and inoculated into 9-mo-old Mdr2−/− mice of the indicated genotype. (F) FACS plots indicating CFSE-positive cells. (G) Percent CFSE-positive cells (n = 5). (H) Coimmunostain for CCL17 (brown) and Foxp3 (red) on liver sections of 11-mo-old Mdr2−/− mice. (Scale bar: 50 μm.) (I) JNP augments tumorigenesis by shaping the inflammatory microenvironment. p-c-Jun, phosphorylated c-Jun.