IL-10-mediated signals act as a switch for lymphoproliferation in Human T-cell leukemia virus type-1 infection by activating the STAT3 and IRF4 pathways
Fig 3
IL-10 induced STAT3-phosphorylation and mild suppression of NF-κB activity in ILTs.
A. Luciferase activities in ILT-H2 and ILT-294 cells containing NF-κB-luc or STAT3-luc and TK-RL reporter genes were measured following incubation with (closed bar) or without (open bar) IL-10 (20 ng/ml) for 48 h. The NF-κB and STAT3 activities were standardized with TK promoter activities, and the relative values against the sample without IL-10 are presented as the mean and SD of duplicate samples. B. The surface IL-10Rα expression (open histogram) on various ILTs was assessed by flow cytometry. The numbers represent relative MFI of IL-10Rα compared with isotype controls (closed histogram). C. ILT cells were cultured with or without IL-10 for two (ILT-294 and -441) or one (ILT-439, -22, -227, and -H2) weeks, and cell lysates were probed with antibodies to phospho-STAT3 (p-STAT3), STAT3, and β-actin in an immunoblotting assay. The numbers under each band represent the relative values of intensity of the band against β-actin. The ratio of the value of p-STAT3 normalized against total STAT3 was also indicated in the bottom of the panel. Representative results of two independent experiments are shown. * p<0.05, ** p<0.01.