American Journal of Reproductive Immunology最新文献

{"title":"Macrophage Polarization and Metabolic Reprogramming in Endometriosis: Mechanisms and Therapeutic Implications","authors":"Leila Adamyan,&nbsp;Igor Malyshev,&nbsp;Laura Pivazyan,&nbsp;Maria Yurkanova,&nbsp;Kristina Kurbatova,&nbsp;Karina Mailova,&nbsp;Assia Stepanian","doi":"10.1111/aji.70331","DOIUrl":"10.1111/aji.70331","url":null,"abstract":"<div>\u0000 \u0000 <p>This review synthesizes evidence on macrophage roles, polarization (M1/M2), and immunometabolic/signaling pathways in endometriosis, outlining therapeutic implications. We searched PubMed, Cochrane Library, ClinicalTrials.gov, Scopus, Embase, and Google Scholar. Available evidence demonstrates increased macrophage accumulation and substantial heterogeneity across the eutopic endometrium, peritoneal fluid, and established endometriotic lesions. Rather than undergoing a uniform shift from an M1 to an M2 phenotype, endometriosis-associated macrophages acquire overlapping inflammatory, immunoregulatory, angiogenic, phagocytic, metabolic, and profibrotic programs. Endometriotic epithelial and stromal cells regulate macrophage recruitment and activation through estrogen receptor β–NF-κB–CCL2 signaling, IL-17A- and TNF-α-dependent cytokine production, extracellular-vesicle-mediated microRNA transfer, and lactate-driven METTL3–Trib1–ERK/STAT3 signaling. The CCL2/MCP-1–CCR2 axis further links monocyte recruitment with inflammatory signaling and the invasive behavior of endometriotic cells, whereas TET3-mediated suppression of let-7 microRNAs sustains disease-associated macrophage activation. Functionally, macrophages contribute to defective clearance of displaced endometrial tissue, ectopic cell survival, angiogenesis, fibrosis, neuroimmune sensitization, pain, and impaired reproductive function. These findings support an immunometabolic model in which macrophage plasticity drives lesion establishment, progression, neuroangiogenesis, pain, and infertility. Therapeutically, targeting macrophage polarization and metabolism—via glycolytic and mitochondrial pathways, lactate signaling, or epitranscriptomic regulators—may restore immune homeostasis and limit disease progression. Further translational studies are needed to validate biomarkers and develop macrophage-directed interventions.</p>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging Role of Galectin-9 in Preventing Preeclampsia in Women With Systemic Mastocytosis","authors":"Syeda Kainat Zehra Rizvi,&nbsp;Hamza Sajid,&nbsp;Mahnoor Batool,&nbsp;Alisha Raza Qureshi,&nbsp;Ahmed Asad Raza","doi":"10.1111/aji.70332","DOIUrl":"10.1111/aji.70332","url":null,"abstract":"","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibrosis and Mechanotransduction in Endometriosis: Linking ECM Remodeling and Tissue Stiffness to Pain","authors":"Hiroshi Kobayashi","doi":"10.1111/aji.70329","DOIUrl":"10.1111/aji.70329","url":null,"abstract":"<div>\u0000 \u0000 <p>Endometriosis is characterized by pain symptoms, including dysmenorrhea, chronic pelvic pain, and dyspareunia, the severity of which does not necessarily correlate with the size or extent of lesions. Recent evidence suggests that, in addition to extracellular matrix (ECM) remodeling and tissue stiffening, neural remodeling and neuroimmune interactions may contribute to pain pathophysiology in endometriotic lesions. This review focuses on the relationship between fibrosis and mechanotransduction in endometriosis. We summarize their associations with inflammation, mechanical stimuli, intracellular signaling pathways, and pain, and examine the possibility that the biomechanical microenvironment of lesions may integrate these pathophysiological processes. Chronic inflammation may promote fibrotic responses, myofibroblast activation, and ECM accumulation. Subsequent ECM remodeling and tissue stiffening can alter cellular tension and activate mechanotransduction pathways. These mechanical signals may interact with inflammatory and neural pathways, potentially promoting neurotrophic factor signaling, sensory nerve remodeling, and nociceptor sensitization. Conversely, neuroimmune signaling may further modulate inflammatory and fibrotic responses, thereby establishing a self-reinforcing microenvironment. However, further investigation is required to determine how these pathophysiological processes differ according to lesion phenotype and anatomical location. In conclusion, pain associated with endometriosis may arise not simply from lesion burden but from dynamic interactions among endocrine, inflammatory, fibrotic, mechanical, and neural processes. The proposed “pain–fibrosis niche” model provides a conceptual framework for integrating these pathophysiological processes and may contribute to the development of mechanism-based and disease-modifying therapeutic strategies.</p>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncovering Placental Endocrine Dysregulation in Gestational Diabetes Mellitus Using Bioinformatics and Machine Learning","authors":"Lijun Deng,&nbsp;Mo Yang,&nbsp;Xin Wang,&nbsp;Ning Gong,&nbsp;Ning Zhang,&nbsp;Qing Yang,&nbsp;Chengmin Gu","doi":"10.1111/aji.70325","DOIUrl":"10.1111/aji.70325","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Gestational diabetes mellitus (GDM) is a common metabolic disorder, posing serious health risks to both mother and fetus. This study aims to explore the placental endocrine mechanisms involved in GDM.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The training dataset GSE203346 and endocrine-related gene sets from the Molecular Signatures Database were used to identify endocrine-related differentially expressed genes (ER-DEGs). Support vector machine recursive feature elimination (SVM-RFE) and Boruta algorithms were employed to identify hub genes. Diagnostic performance was analyzed using the receiver operating characteristic (ROC) curves. Immune cell infiltration was evaluated using the CIBERSORT algorithm, followed by single-gene gene set enrichment analysis (GSEA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 57 ER-DEGs were identified in the GDM placental samples. Machine learning identified nine important genes, of which CACNA1C, CCDC102B, and KIF21A exhibited high diagnostic performance (AUC &gt; 0.80) in two external validation datasets (GSE154414 and GSE255075). Immune infiltration analysis revealed potential differences in several immune cell proportions between high- and low-expression groups of the hub genes. High expression of CACNA1C, CCDC102B, and KIF21A was associated with the Notch pathway, mTOR pathway, and autophagy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>CACNA1C, CCDC102B, and KIF21A may be the potential biomarkers and therapeutic targets for GDM.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal SARS-CoV-2 Infection and Neonatal Immune Profiles: Clarifying Post-Exposure Obstetric Adjustment","authors":"Ercan Yılmaz","doi":"10.1111/aji.70328","DOIUrl":"10.1111/aji.70328","url":null,"abstract":"","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the Silent Endometrium: Dysbiosis, Immune Subversion and Antimicrobial Resistance in Chronic Endometritis: A Narrative Review.","authors":"Ahmed Wael Moftah","doi":"10.1111/aji.70337","DOIUrl":"https://doi.org/10.1111/aji.70337","url":null,"abstract":"<p><p>Chronic endometritis (CE) represents an insidious and frequently underdiagnosed inflammatory condition of the endometrial stroma, increasingly recognized as a principal contributor to unexplained infertility, recurrent implantation failure and recurrent pregnancy loss. Historically relegated to a histological curiosity, CE has been reframed as a biologically complex disorder characterized by the convergence of endometrial microbial dysbiosis, immunological subversion, and, increasingly, antimicrobial resistance (AMR). This narrative review synthesizes contemporary evidence examining the mechanistic interplay between aberrant endometrial microbiota composition, disrupted innate and adaptive immune responses, and the emergence of antibiotic-resistant endometrial pathogens, collectively undermining endometrial receptivity and embryo implantation. We critically appraise the diagnostic limitations inherent to current histological and microbiological standards, and examine the translational implications of next-generation sequencing for the characterization of the endometrial microbiome. Furthermore, we interrogate the therapeutic paradox posed by AMR in clinical CE management, and delineate future research trajectories encompassing microbiome-targeted therapeutics, immunomodulatory strategies, and the ethical dimensions of emerging diagnostic and treatment frameworks. A convergent pathophysiological model is proposed in which microbial dysbiosis, immune dysregulation, and AMR form a self-reinforcing axis of reproductive failure, demanding integrated diagnostic and therapeutic paradigms.</p>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":"e70337"},"PeriodicalIF":2.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BeWo-Derived Extracellular Vesicles Downregulate IL-6Rα Expression via miRNAs on CD4+ T Lymphocytes.","authors":"Gábor Seregélyes, Bence Nagy, Árpád Ferenc Kovács, Nóra Fekete, Edit I Buzás, Éva Pállinger","doi":"10.1111/aji.70335","DOIUrl":"10.1111/aji.70335","url":null,"abstract":"<p><strong>Problem: </strong>A balanced Th1/Th2/Th17/Treg status is necessary for a successful pregnancy. T cell polarization depends on the local cytokine environment and the responsiveness of T lymphocytes to cytokines. Trophoblast-derived extracellular vesicles (EVs) influence the function of maternal T lymphocytes, contributing to their polarization into the Treg phenotype. We examined whether BeWo-derived EVs affect T cell IL-6 responsiveness using the BeWo cell line as an experimental model and characterized the molecular cargo of BeWo -EVs that may contribute to this process.</p><p><strong>Methods: </strong>Circulating lymphocytes from non-pregnant women were treated with BeWo-EVs or co-cultured with BeWo cells. We detected IL-6Rα expression by flow cytometry and IL6R signaling pathways by RT-PCR. The microRNA (miRNA) content of BeWo EVs was identified by sequencing. Finally, we compared IL-6Rα expression levels in circulating T lymphocytes from healthy pregnant and non-pregnant women.</p><p><strong>Results: </strong>BeWo-EVs reduced IL-6Rα expression on CD4+ T cells. This modifies the IL-6 pathway by downregulating the transcription factors STAT3, NFKB1, and PIAS3 while upregulating STAT1. This may be due to the presence of specific microRNAs (miRNAs), such as hsa-mir-92a-3p, hsa-mir-520f-3p, and hsa-mir-25-3p, in BeWo-EVs that target the IL-6 pathway. Treatment with BeWo-EVs also induced phenotypic and functional changes in T cells and enhanced the ratio of CD4+/CD25+ T cells that produce IL-10. Pregnancy-associated IL-6Rα downregulation has been demonstrated in clinical samples. Significantly lower levels of IL-6Rα were detected on circulating CD4+CD25+ T cells in healthy pregnant women compared to healthy non-pregnant individuals.</p><p><strong>Conclusions: </strong>Our studies suggest that the microRNA content of trophoblast-derived EVs significantly influences the local polarization of maternal T lymphocytes by modifying the IL-6Rα signaling pathway.</p>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":"e70335"},"PeriodicalIF":2.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13677083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of MHC- and TCR-Like Immunoreactivity With Sperm Parameters in Human Semen","authors":"Paraskevi Xystra,&nbsp;Theologia Morfoniou,&nbsp;Tania Antonopoulou,&nbsp;Aliki Anyfantaki,&nbsp;Katerina Vardaki,&nbsp;Mattheos Fraidakis,&nbsp;Irene Athanassakis","doi":"10.1111/aji.70327","DOIUrl":"https://doi.org/10.1111/aji.70327","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Since the expression of MHC and TCR molecules in murine semen was correlated to fertility, the present study focused in humans and inquired whether the complementarity of MHCs and TCRs could affect sperm quality through sperm morphology and motility.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>Sixty sperm-donor samples engaged in assisted reproduction processes were examined as to sperm quality and ability to fertilization. Semen was examined for membrane MHC class I (MHCI), class II (MHCII), TCR<i>αβ</i> and TCRγδ molecule expression by immunofluorescence followed by electron/confocal microscopy or flow cytometry analysis, while the presence of their soluble forms in seminal plasma was examined using ELISA. TCR<i>αβ</i>-isolates from seminal plasma were submitted to SDS-PAGE analysis and ELISA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All samples expressed membrane and soluble MHCI, MHCII, TCR<i>αβ</i> and TCRγδ molecules in spermatozoa and seminal plasma in a statistically significant one-way ANOVA repeated measure analysis. The expression was localized in spermatozoa head accompanied in most cases by tail staining, correlating with coiled-tail morphology. The distinction of samples into good-quality fertilizing, good-quality non-fertilizing and bad-quality non-fertilizing sperm showed statistically significant difference of MHCI, TCR<i>αβ</i> and TCRγδ in the fertilizing as compared to non-fertilizing groups. Evaluating already known parameters, significant increase of macrophage-migration inhibitory factor (MIF) in seminal plasma and decrease of nitric oxide were detected in fertilizing as compared to non-fertilizing samples. Seminal plasma-derived TCR<i>αβ</i> co-precipitated with MIF, resembling thus T-suppressor-Factor-1.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The results correlate polymorphic immune molecules in spermatozoa and seminal plasma with sperm morphology and motility, introducing novel parameters and research areas in sperm quality evaluation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vaginal Lactic Acid and Lactobacillus-Dominated Microbiota in HIV-1 Susceptibility: Mechanistic Insights and Implications for Sub-Saharan African Women","authors":"Aziz Adamu","doi":"10.1111/aji.70326","DOIUrl":"https://doi.org/10.1111/aji.70326","url":null,"abstract":"<div>\u0000 \u0000 <p>Women in Sub-Saharan Africa experience disproportionately high rates of HIV-1 acquisition, a disparity not fully explained by reported sexual behavior or conventional epidemiological risk factors. Increasing evidence implicates the cervicovaginal microbiome, particularly the presence of a Lactobacillus-dominated, lactic-acid-rich environment, as an important biological determinant of susceptibility. This review synthesizes mechanistic, clinical, and epidemiological evidence linking vaginal lactic acid, Lactobacillus-dominated microbiota, bacterial vaginosis, and HIV-1 acquisition, with particular emphasis on evidence from African populations. Lactic acid produced by vaginal Lactobacillus spp. exhibits direct anti-HIV-1 activity, suppresses bacterial-vaginosis-associated organisms, and contributes to epithelial barrier homeostasis. Conversely, anaerobe-dominated dysbiosis is associated with reduced lactic acid production, epithelial disruption, heightened inflammatory signaling, and increased availability of HIV-1 target cells, with African cohorts reporting approximately two- to four-fold greater HIV-1 acquisition risk among women with dysbiotic microbiota. Emerging interventions targeting vaginal microbiota, including Lactobacillus crispatus-based live biotherapeutics, demonstrate potential to restore microbiological homeostasis and reduce bacterial vaginosis recurrence. Collectively, the evidence supports vaginal microbial restoration as a biologically plausible adjunct to HIV-1 prevention. However, regionally validated trials, durable microbiome-targeted interventions, scalable diagnostics, and integration with established prevention platforms are needed to determine clinical effectiveness and implementation feasibility in high-burden African settings.</p>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal-Fetal Interplay During Mid-gestation: Inflammatory Biomarker Levels in Maternal Sera, Cord Sera and Placenta","authors":"Dana E. Goin,&nbsp;Lin Li,&nbsp;Stephanie L. Gaw,&nbsp;Rachel Morello-Frosch,&nbsp;Tracey J. Woodruff,&nbsp;Stephanie M. Eick,&nbsp;Joshua F. Robinson","doi":"10.1111/aji.70324","DOIUrl":"https://doi.org/10.1111/aji.70324","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Maternal inflammation is linked to adverse maternal and fetal outcomes, but how maternal inflammation affects fetal inflammation during mid-gestation is not known.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>We measured 20 biomarkers of inflammation, including chemokines, pro-and anti-inflammatory cytokines, and immunomodulatory cytokines, in matched maternal and cord sera and placental tissue collected during the second trimester from a diverse cohort (<i>N</i> = 106). We examined trends in biomarkers across the second trimester using a linear trend test, and compared distributions across sociodemographic groups using a Kruskal-Wallis test. We calculated Spearman correlation coefficients and stratified the correlation matrices by gestational age at sample collection (&lt;20 vs. ≥ 20 gestational weeks).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Most inflammatory biomarkers did not exhibit clear trends with gestational age, except for cord levels of CCL17 and CCL22; both Th2-associated chemokines significantly increased across the second trimester. There were no consistent patterns in biomarker levels across sociodemographic groups. Overall, correlations among maternal, placental and cord biomarkers were stronger before 20 weeks’ gestation than in later pregnancy. While correlations between maternal and placental CCL17 declined after 20 weeks, the correlation between placental and cord CCL17 increased during this same period.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Maternal and fetal inflammatory responses are more tightly coordinated earlier in the second trimester.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 3","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70324","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}