ReviewJournal of clinical medicine2024
Maternal-Fetal Compatibility in Recurrent Pregnancy Loss.
Review in Journal of clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- The Role of Granulocyte Colony Stimulating Factor in Mitigating the Risk of Recurrent Miscarriages: A Comprehensive Review and Meta-Analysis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Pooled it
- Miscarriage and the Microbiome: Host Genetics, Immunity, and the Reproductive Tract Ecosystem.Genes · 2026Review
- Artificial Intelligence in Recurrent Pregnancy Loss: Current Evidence, Limitations, and Future Directions.Journal of clinical medicine · 2026Review
- Parental KIR/HLA-C Profiles and Reproductive Failure: A Phenotype-Stratified Retrospective Analysis of Couples With Fertility Disorders.Obstetrics and gynecology international · 2026Article
- Causal effects of maternal BMI on pregnancy outcomes: a Mendelian randomisation study investigating the mediating role of blood counts.Frontiers in genetics · 2026Article
- dNK3 cells in normal pregnancy and recurrent pregnancy loss: from molecular identity to functional imbalance.Frontiers in immunology · 2026Review
- The non-classical immune checkpoint HLA-G: a regulatory master switch governing tolerance, evasion, and translational frontiers.Frontiers in oncology · 2026Review
- Immunological Causes of Infertility: Diagnostic Perspectives.Biomolecules · 2025Review
- Immunotherapy and IVF Outcomes in Unexplained Recurrent Pregnancy Loss: A Systematic Review with Implications for Personalized Reproductive Medicine.Journal of personalized medicine · 2025Review
- Review
- Alloimmune Causes of Recurrent Pregnancy Loss: Cellular Mechanisms and Overview of Therapeutic Approaches.Medicina (Kaunas, Lithuania) · 2024Review
- "Unraveling the Clot-Miscarriage Nexus: Mechanisms, Management, and Future Directions in Thrombosis-Related Recurrent Pregnancy Loss".Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nowadays, recurrent pregnancy loss (RPL) is an undesirable condition suffered by many patients of reproductive age. In this scenario, certain immune cell populations and molecules, involved in maternal-fetal compatibility, have emerged as factors related with the pathogenesis of RPL. Among them, uterine Natural Killer cells (uNKs) appear to be of great relevance. These cells are involved in numerous processes during pregnancy, such as the remodeling of uterine spiral arteries or the control of trophoblast invasion. These functions are regulated by the interactions that these cells establish with the extravillous trophoblast, mainly through their Killer Immunoglobulin-like Receptors (KIRs) and the Human Leukocyte Antigen-C (HLA-C) molecules expressed by the embryo. A high level of polymorphism has been reported for both molecules involved in this interaction, with some of the possible KIR-HLA-C combinations being associated with an increased risk of RPL. However, the complexity of the maternal-fetal interface goes beyond this, as other HLA molecules also appear to be related to this reproductive pathology. In this review, we will discuss the role of uNKs in pregnancy, as well as the polymorphisms and clinical implications of KIR-HLA-C binding. We will also address the involvement of other, different HLA molecules in RPL, and the current advice on the appropriate management of patients with 'immunological mismatch', thus covering the main aspects regarding the involvement of maternal-fetal compatibility in RPL.
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.