ArticleMolecular and cellular biochemistry2025
Immune dysregulation of decidual NK cells mediated by GRIM19 downregulation contributes to the occurrence of recurrent pregnancy loss.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Partial embryo loss caused by disruption of the placental hormone CTRP6 coincides with dNK cell abnormalities during pregnancy.iScience · 2026Article
- The role of dendritic cells in recurrent pregnancy loss.Immunologic research · 2025Review
- From gut dysbiosis to decidual hostility: the immuno-metabolic crosstalk driving recurrent pregnancy loss.Frontiers in immunology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
In patients with recurrent pregnancy loss (RPL), excessive activation of decidual natural killer (dNK) cells has been widely observed, yet the precise underlying mechanisms remain to be elucidated. We collected decidual specimens from RPL patients and controls to assess GRIM19 expression, activation phenotype, cytotoxic function, inflammatory cytokine secretion, and mitochondrial homeostasis in dNK cells. Furthermore, we established a GRIM19-knockout NK-92MI cell line and a GRIM19 ± C57BL/6J mouse model to investigate the relationship between GRIM19 downregulation and dNK immune dysregulation, ultimately contributing to pregnancy loss. Decidual NK cells from RPL patients exhibited significantly lower GRIM19 expression, accompanied by abnormal hyperactivation, enhanced cytotoxicity, and abnormal mitochondrial activation. In vitro experiments confirmed that reduced GRIM19 expression significantly potentiated the cytotoxicity and pro-inflammatory cytokine secretion of NK-92MI cells, while also promoting mitochondrial homeostasis imbalance. Mouse model studies corroborated that GRIM19 downregulation triggers NK cell homeostasis imbalance, contributing to the occurrence of pregnancy loss. Downregulation of GRIM19 in dNK cells contributes to RPL through hyperactivation and disruption of mitochondrial homeostasis, emphasizing its potential as a diagnostic and therapeutic target.
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