Abstract
Lipid metabolism is altered in several cancer settings leading to different ratios of intermediates. Ovarian cancer is the most lethal gynecological malignancy. Cancer cells disperse in the abdominal space and ascites occurs. T cells obtained from ascites are unable to proliferate after an antigenic stimulus. The proliferation of ascites-derived T cells can be restored after culturing the cells for ten days in normal culture medium. No pathway aberrancies were detected. The acellular fraction of ascites can inhibit the proliferation of autologous as well as allogeneic peripheral blood lymphocytes, indicating the presence of soluble factors that interfere with T cell functionality. Therefore, we analyzed 109 lipid mediators and found differentially regulated lipids in suppressive ascitic fluid compared to normal abdominal fluid. Our study indicates the presence of lipid intermediates in ascites of ovarian cancer patients, which coincidences with T cell dysfunctionality. Since the immune system in the abdominal cavity is compromised, this may explain the high seeding efficiency of disseminated tumor cells. Further research is needed to fully understand the correlation between the various lipids and T cell proliferation, which could lead to new treatment options.
Highlights
Worldwide, more than 239,000 women per year are diagnosed with ovarian cancer and 152,000 succumb annually [1,2]
Peripheral blood lymphocytes (PBLs) from healthy individuals had higher proliferation rates when stimulated with increasing concentrations of αCD3/28 beads
Since patient-derived cells produced more IFN-γ when stimulated with IL-12, we reasoned that IL-2 unresponsiveness might be the cause for the observed hypo proliferation
Summary
More than 239,000 women per year are diagnosed with ovarian cancer and 152,000 succumb annually [1,2]. Mesothelial cells, and macrophages; tumor cells and; in the case of rapid fluid development, a high proportion of red blood cells. T cell immunity in the tumor microenvironment has a profound impact on ovarian cancer outcome and plays a significant role in controlling recurrence [4,5]. Tumor cells can escape destruction by the immune system in several ways. Accumulation of Tregs at the tumor site is associated with reduced survival of ovarian cancer patients, as are high CD4/CD8 ratios. CD8+ effector T cells are inhibited by tumor macrophages expressing B7-H4 [9,10]. Patients with a high CD4/CD8 ratio have a poorer outcome, whereas a high tumor infiltrating lymphocytes (TIL)/Treg ratio is generally favorable [10]
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