PROBLEM: MUC16 (CA125) released from ovarian tumors binds to NK cells and monocytes via the inhibitory receptor Siglec-9. Here, we investigate whether MUC16 also binds to circulating immune cells during pregnancy and in women with preeclampsia. METHOD OF STUDY: MUC16 binding was monitored by flow cytometry and immunoprecipitation, and RT-PCR was used to monitor indigenous expression in immune cells. Serum CA125 levels were measured by a clinical assay. RESULTS: MUC16 was equally distributed on Siglec-9(pos) CD16(pos)/CD56(dim) and CD16(neg)/CD56(br) NK cells in the healthy pregnant and preeclampsia groups. While serum CA125 levels and number of NK and monocytes were similar, increased binding of MUC16 was observed on these immune cells in the preeclampsia cohort as compared to the healthy pregnant samples. CONCLUSION: MUC16 binding to NK cells and monocytes likely contributes to tolerance of the fetal allograft from maternal responses and may also serve as a novel biomarker for preeclampsia.
PROBLEM: MUC16 (CA125) released from ovarian tumors binds to NK cells and monocytes via the inhibitory receptor Siglec-9. Here, we investigate whether MUC16 also binds to circulating immune cells during pregnancy and in women with preeclampsia. METHOD OF STUDY: MUC16 binding was monitored by flow cytometry and immunoprecipitation, and RT-PCR was used to monitor indigenous expression in immune cells. Serum CA125 levels were measured by a clinical assay. RESULTS:MUC16 was equally distributed on Siglec-9(pos) CD16(pos)/CD56(dim) and CD16(neg)/CD56(br) NK cells in the healthy pregnant and preeclampsia groups. While serum CA125 levels and number of NK and monocytes were similar, increased binding of MUC16 was observed on these immune cells in the preeclampsia cohort as compared to the healthy pregnant samples. CONCLUSION:MUC16 binding to NK cells and monocytes likely contributes to tolerance of the fetal allograft from maternal responses and may also serve as a novel biomarker for preeclampsia.
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