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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Cancer Immunol Res. 2016 Jan 27;4(4):303–311. doi: 10.1158/2326-6066.CIR-15-0157

Figure 1.

Figure 1

Type-1 activation of immune cells within the bulk ovarian cancer tumor microenvironment enhances local MDSC-mediated expression of suppressive factors. (A) Bulk ascites cells freshly-isolated from ovarian cancer (OvCa) patients were lysed and analyzed for expression of type-1 immune markers (CD8α, NKG2D, and IFNγ) and COX2. Data are expressed as ratios between the expression of individual genes and HPRT1, and represent 15 independent patients. (B) Bulk OvCa ascites cells were cultured for 24 h in the absence or presence of the NK cell-activating (NKact) stimuli IL18/IFNα or the CD8+ T cell–activating (CD8act) stimuli anti-CD3/IL12, and analyzed for expression of IFNγ, TNFα, IDO1, NOS2, IL10, and COX2. Data are expressed as ratios between the expression of individual genes and HPRT1, and shown as the mean expression (± SD) of triplicate cultures. Data represent one of three independent experiments, all yielding similar results. (C) Bulk OvCa ascites cells or ascites cells depleted of CD56+ NK cells (NKdeplete) were cultured for 24 h in the absence or presence of the NK cell-activating (NKact) stimuli IL18/IFNα, and analyzed for expression of IDO1, NOS2, IL10, and COX2. Data are expressed as ratios between the expression of individual genes and HPRT1, and represent 4 independent patients. (D) Bulk OvCa ascites cells or ascites cells depleted of MDSCs (MDSCdeplete) were cultured for 24 h in the absence or presence of the NK cell–activating (NKact) stimuli IL18/IFNα, and analyzed for expression of IDO1, NOS2, IL10, and COX2. Data are expressed as ratios between the expression of individual genes and HPRT1, and represent 3 independent patients. ***P < 0.001, ** P < 0.01, * P < 0.05, ns: P > 0.05 compared to indicated group or compared to all groups when not specifically indicated.