Frontiers in immunology · 2026
Downregulation of CD200 in the placenta of preeclampsia: a potential regulator of macrophage-mediated immune imbalance at the maternal-fetal interface.
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Huang Shuzhen, Yang Zhaowen, Li Zijian, Liang Quanqi, Xiao Zheng, Yang Heng, Chen Yongkun, Wen Suiwen, Li Kaishu, Peng Cui
Аннотация
OBJECTIVE: To investigate the role and potential mechanism of CD200 in the pathogenesis of preeclampsia (PE) and to clarify its potential value as a biomarker candidate and possible therapeutic target for PE.
METHODS: This retrospective study enrolled 57 patients with PE and 49 women with normal full-term pregnancies. Clinical data were collected, and serum biomarkers were measured. The GSE93839 dataset was utilized to screen for differentially expressed genes in PE placental tissues. Hematoxylin-eosin (HE) staining, immunohistochemistry (IHC), and immunofluorescence (IF) techniques were employed to analyze the expression and localization characteristics of CD200 in placental tissues. Exploratory path analysis was conducted to investigate potential indirect associations between CD200 expression and PE through serum biomarkers.
RESULTS: Bioinformatics analysis identified CD200 as a candidate downregulated gene associated with PE. Immunohistochemistry revealed a significantly lower expression level of CD200 in the placental tissues of PE patients (p < 0.05). Immunofluorescence experiments demonstrated co-localization of CD200 with CD68+ macrophages, suggesting a potential association with macrophage-related immune regulation at the maternal-fetal interface. Exploratory path analysis revealed statistically significant indirect associations between CD200 expression and PE through serum biomarkers, including high-density lipoprotein cholesterol (HDL-C), albumin, alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB) (p < 0.05).
CONCLUSION: The expression of CD200 is significantly downregulated in the placental tissues of PE patients. This alteration may induce immune imbalance at the maternal-fetal interface and placental dysfunction, and may also be linked to the systemic pathological injury process in PE through its associations with multiple serum biomarkers.
METHODS: This retrospective study enrolled 57 patients with PE and 49 women with normal full-term pregnancies. Clinical data were collected, and serum biomarkers were measured. The GSE93839 dataset was utilized to screen for differentially expressed genes in PE placental tissues. Hematoxylin-eosin (HE) staining, immunohistochemistry (IHC), and immunofluorescence (IF) techniques were employed to analyze the expression and localization characteristics of CD200 in placental tissues. Exploratory path analysis was conducted to investigate potential indirect associations between CD200 expression and PE through serum biomarkers.
RESULTS: Bioinformatics analysis identified CD200 as a candidate downregulated gene associated with PE. Immunohistochemistry revealed a significantly lower expression level of CD200 in the placental tissues of PE patients (p < 0.05). Immunofluorescence experiments demonstrated co-localization of CD200 with CD68+ macrophages, suggesting a potential association with macrophage-related immune regulation at the maternal-fetal interface. Exploratory path analysis revealed statistically significant indirect associations between CD200 expression and PE through serum biomarkers, including high-density lipoprotein cholesterol (HDL-C), albumin, alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB) (p < 0.05).
CONCLUSION: The expression of CD200 is significantly downregulated in the placental tissues of PE patients. This alteration may induce immune imbalance at the maternal-fetal interface and placental dysfunction, and may also be linked to the systemic pathological injury process in PE through its associations with multiple serum biomarkers.