ReviewFrontiers in immunology2026
dNK3 cells in normal pregnancy and recurrent pregnancy loss: from molecular identity to functional imbalance.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Decidual natural killer (dNK) cells constitute approximately 70% of first-trimester decidual leukocytes and play critical roles in immune tolerance, angiogenesis, and trophoblast invasion. Single-cell RNA sequencing has revealed substantial heterogeneity within the dNK population, identifying three major subsets-dNK1, dNK2, and dNK3-with distinct transcriptomic profiles and predicted functions. dNK3 Characteristics: dNK3 cells are characterized by a CD160 Clinical relevance: Multiple independent studies have identified a reproducible dNK1-down/dNK3-up shift in recurrent pregnancy loss (RPL), with dNK3 cells showing IFNG upregulation at chromatin, transcriptional, and protein levels. This subset imbalance positions the dNK1/dNK3 ratio as a candidate diagnostic biomarker and identifies potential therapeutic targets including M-CSF supplementation, TGF-β pathway modulation, and iPSC-derived dNK cell therapy. Conclusions: While dNK3 represents a promising focus for reproductive immunology and RPL, the current evidence base remains insufficient for clinical translation. Critical questions regarding causality, cross-study comparability, and the dNK3/ieILC1 developmental relationship require resolution through prospective cohorts and rigorous functional validation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.