AI Article Synopsis

  • Peritoneal ascites in advanced epithelial ovarian cancer (EOC) show varied lymphocyte subsets and may contain malignant cells.
  • The study focused on assessing the functionality of natural killer (NK) cells in ascites, observing that NK cells from EOC cell-free ascites exhibited higher degranulation activity compared to those from ascites with EOC cells.
  • Regulatory T cells and tumor necrosis factor (TNF)-α levels were elevated in ascites containing EOC cells, indicating a more immunosuppressive environment and impaired NK cell response.

Article Abstract

Peritoneal ascites are a distinguishable feature of patients with advanced epithelial ovarian cancer (EOC). The presence of different lymphocyte subsets has been reported in EOC-associated ascites, which also can or not contain malignant cells. The goal of this study was to analyze the functional characteristics of natural killer (NK) cells from EOC-associated ascites in terms of their expression of activating receptors and ascites' contents of lymphocyte subtypes, cytokine profile and presence of EOC cells. NK cell function was evaluated by the expression of the degranulation marker CD107a in resting and interleukin (IL)-2 stimulated NK cells from ascites and blood. Degranulation of NK cells from EOC cell-free ascites was significantly ( < 0.05) higher than all the other groups, either in their resting state or after IL-2 stimulation, suggesting a previous local stimulation. In contrast, treatment with IL-2 had no effect on NK cells from ascites with EOC cells. The amount of regulatory T cells was significantly higher in ascites with EOC cells compared to EOC cell-free ascites. Ascites with EOC cells also had higher levels of tumor necrosis factor (TNF)-α, suggesting inflammation related to the malignancy. In conclusion, the functional performance of NK cells was distinct between EOC cell-free ascites and ascites with EOC cells. The impairment of NK cell response to IL-2 in ascites with EOC cells was consistent with an immunosuppressive tumor microenvironment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5454809PMC
http://dx.doi.org/10.3390/ijms18050856DOI Listing

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