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. 2018 Mar 15;7(5):e1424672. doi: 10.1080/2162402X.2018.1424672

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© 2018 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 4. — Ovarian carcinoma ascites suppresses function of CD8⁺ T_EM cells. (A) Flow cytometry analysis of PLCγ1 and transcription factors STAT5B and NFATc2 associated with TCR- and IL-2-signaling in activated CD8⁺ T_EM cells from healthy donors (n = 3). Median fluorescence intensity (MFI) is shown. The gating strategy and histograms are shown in Figure S5. (B, C) Flow cytometry analysis of intracellular TNF-α-positive cells (%) and CD107a (MFI) in activated CD8⁺ T_EM cells from healthy donors (n = 3 per group). The gating strategy and histograms are shown in Figure S6. Statistical analysis by t-test: ***: p < 0.001, **: p < 0.01: *p < 0.05, n.s.: not significant (ascites groups considered as one group with n = 9). (D) A model integrating diverse effects of the ovarian cancer environment on the accumulation and function of CD8⁺ T_EM cells. TAM (and to some extent other cell types) attract CXCR3-expressing T_EM cells from the periphery via secretion of CXCL9, CXCL10 and CXCL11 chemokines (and possibly other mediators). However, once migrated into the tumor microenvironment (TME) the activation and function of these T_EM cells is suppressed by mediators of tumor environment, thus causing shortened RFS of patients. This is in part mediated by lowering the expression levels of signal transduction proteins crucial for T cell activation.