ArticleClinical and translational medicine2025
Granulocyte colony-stimulating factor induced T-cell hyporesponsiveness via modulation of CD177
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Granulocyte colony-stimulating factor induced T-cell hyporesponsiveness via modulation of CD177Clinical and translational medicine · 2025Article
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3 authors.
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Abstract
backgroundNumerous studies have demonstrated the promising efficacy of granulocyte colony-stimulating factor (G-CSF) in the treatment of couples with unexplained recurrent pregnancy loss (URPL) during early pregnancy. While neutrophils are recognised as the main effectors mediating immunoregulation, their G-CSF-mobilised phenotype and mechanisms regulating maternal-fetal immunity remain unclear.
methodsSingle-cell RNA sequencing (scRNA-seq) and single-cell T-cell receptor sequencing (scTCR-seq) were conducted to uncover the immune reconstitution dynamics of peripheral blood under G-CSF stimulation. Integrative analysis of transcriptomic-proteomic profiles with functional validation revealed a unique immunomodulatory neutrophil population. Further, we used spatial transcriptomics, flow cytometry and immunohistochemistry to explore the spatial distribution characteristics of this population at the maternal-fetal interface, and validated its therapeutic efficacy in animal models.
resultsG-CSF-mobilised peripheral blood (G-PB) displayed immune hyporesponsiveness. Unique neutrophils expressing high levels of CD177 and the S100A gene family expanded substantially in response to G-CSF. These neutrophils exhibited a comparatively immature morphology and impaired T-cell responses via contact-dependent arginase 1 release, as well as upregulation of T-cell immune checkpoints. A reduction of CD177
conclusionG-CSF played a crucial regulatory role in improving pregnancy outcomes by selectively expanding CD177⁺S100A KEY POINTS: G-CSF induces peripheral blood immune hyporesponsiveness in patients with UPRL. First to characterize G-CSF mobilised CD177
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