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Free Content Peritoneal natural killer cells from epithelial ovarian cancer patients show an altered phenotype and bind to the tumour marker MUC16 (CA125)

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Summary

The ovarian tumour marker MUC16 (CA125) inhibits the cytotoxic responses of human natural killer (NK) cells and down-regulates CD16. Here we show that approximately 10% of the peripheral blood NK cells (PBNK) from the epithelial ovarian cancer (EOC) patients are CD16 CD56br whereas 40% of the peritoneal fluid NK (PFNK) carry this phenotype, which is usually associated with NK cells from the lymph nodes or human decidua. PBNK from healthy donors exposed to PF show a significant increase in the CD16 CD56br population. This shift in phenotype is not caused by increased apoptosis of the CD16+ CD56dim cells or selective proliferation of the CD16 CD56br NK cells. Thus, the terminal differentiation of the CD16 CD56br NK cells to CD16+ CD56dim subset that occurs during normal NK cell development may actually be a reversible step. A majority of the NK cell receptors (NKp46, NKp44, NKG2D, CD244, CD226, CD158a, CD158b, and CD158e) studied were down-regulated in the PFNK. MUC16 binds selectively to 30–40% of CD16+ CD56dim NK cells in EOC patients indicating that phenotypic alterations in these cells are mediated by tumour-derived soluble factors. Similar to EOC, MUC16 in early pregnancy also binds to NK cells suggesting shared mechanisms of NK cell suppression in feto-maternal tolerance and immune evasion by ovarian cancers.
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Keywords: CA125; MUC16; immune suppression; natural killer; ovarian cancer

Document Type: Research Article

Affiliations: 1: Department of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI, USA 2: Department of Microbiology and Infectiology, Université de Sherbrooke, Sherbrooke, Canada

Publication date: November 1, 2007

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