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Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human leukocyte antigen-C (HLA-C)/killer immunoglobulin-like receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.

Journal: Frontiers in Immunology

Article Title: Multi-omics insights into immune tolerance at the maternal–fetal interface in recurrent pregnancy loss: mechanisms, integration challenges, and translational perspectives

doi: 10.3389/fimmu.2026.1811970

Figure Lengend Snippet: Disrupted cellular interaction network at the maternal–fetal interface in recurrent pregnancy loss (RPL). This schematic illustrates representative alterations in cell–cell communication associated with immune tolerance failure at the maternal–fetal interface. Under pathological conditions, impaired decidual stromal cell (DSC)-derived transforming growth factor-β (TGF-β) signaling may contribute to loss of the tolerogenic uterine natural killer (uNK) cell phenotype. Reduced Galectin-9 signaling and abnormal uNK–human leukocyte antigen-C (HLA-C)/killer immunoglobulin-like receptor (KIR) interactions may weaken trophoblast support. In parallel, macrophage polarization may shift toward a pro-inflammatory M1-like state, and the balance between regulatory T cells (Treg) and T helper 17 (Th17) cells may become disrupted. These alterations are associated with impaired trophoblast support and increased susceptibility to trophoblast stress and apoptosis. This figure is intended as a conceptual summary of reported cellular interaction abnormalities rather than a definitive mechanistic model. DSCs, decidual stromal cells; FASL, Fas ligand; HLA-C, human leukocyte antigen-C; KIR, killer cell immunoglobulin-like receptor; TGF-β, transforming growth factor-β; Th17, T helper 17 cells; TNFRs, tumor necrosis factor receptors; Treg, regulatory T cells; uNK, uterine natural killer cell.

Article Snippet: Furthermore, abnormal uNK–trophoblast interactions have been associated with reduced Galectin-9 expression and imbalanced killer immunoglobulin-like receptor (KIR)–human leukocyte antigen-C (HLA-C) pairing, which may impair trophoblast invasiveness and endothelial remodeling, ultimately contributing to defective spiral artery remodeling and placental perfusion disorders ( , ).

Techniques: Derivative Assay