Decidual infiltration of FoxP3+ regulatory T cells, CD3+ T cells, CD56+ decidual natural killer cells and Ki-67 trophoblast cells in hydatidiform mole compared to normal and ectopic pregnancies
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- Published online on: October 14, 2011 https://doi.org/10.3892/mmr.2011.633
- Pages: 275-281
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Abstract
Hydatidiform moles are considered pre-cancerous lesions of gestational trophoblastic neoplasia and are associated with an aberrant immune response. This preliminary study aimed to evaluate the feasibility of measuring the presence of immune cells as potential prognostic markers for hydatidiform moles. Immunohistochemical staining of FoxP3+ regulatory T cells, CD3+ T cells, CD56+ decidual natural killer cells and Ki-67+ trophoblast cells was performed on 32 samples. Samples were from complete hydatidiform moles, partial hydatidiform moles, ectopic pregnancies, gestational age-matched normal elective pregnancy terminations (normal pregnancies) and gestational trophoblastic neoplasias. FoxP3+ regulatory T-cell infiltration was highest in the complete hydatidiform moles and lowest in the normal pregnancy samples. The normal pregnancy cases showed significantly fewer FoxP3+ regulatory T cells compared to the ectopic pregnancy cases (p=0.037) and compared to the combination of all of the other groups (p=0.044). Normal pregnancy samples also showed the lowest infiltration of CD3+ T cells and the highest number of CD56+ decidual natural killer cells; conversely, gestational trophoblastic neoplasias showed the highest infiltration of CD3+ T cells and the lowest number of CD56+ decidual natural killer cells. The numbers of Ki-67+ trophoblast cells were highest in the gestational trophoblastic neoplasias (688/1,000 trophoblast cells) and lowest in the partial moles (87/1,000 trophoblast cells). Our results suggest that regulatory T cells may be involved in the progression of complete hydatidiform moles. A larger cohort study is required to assess whether immune cells are effective prognostic markers in gestational trophoblastic diseases.