American Journal of Reproductive Immunology最新文献

{"title":"Correction to “Comment on “Distinct Suppression of Prednisone on Endometrial Immune Cells in Women With Reproductive Failure””","authors":"","doi":"10.1111/aji.70297","DOIUrl":"https://doi.org/10.1111/aji.70297","url":null,"abstract":"<p>J. Linxi, L. Shiling, and Z. Hongli et al., “Comment on “Distinct Suppression of Prednisone on Endometrial Immune Cells in Women With Reproductive Failure”” <i>American Journal of Reproductive Immunology</i> 94, no. 5 (2025): e70186, https://doi.org/10.1111/aji.70186.</p><p>In the article, there is an error in author affiliation.</p><p>The incorrect affiliation reads:</p><p>Zhejiang Hospital of Traditional Medicine, Zhejiang, China</p><p>The correct affiliation reads:</p><p>Hangzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University.</p><p>We apologize for this error.</p>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70297","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148783988","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":"Interleukin-1 Receptor Accessory Protein Amplifies Trophoblast Inflammatory Signaling in Inflammation-Associated Preterm Birth","authors":"Jasmine Edghill,&nbsp;Busra Cetinkaya-Un,&nbsp;Jessica Lynch,&nbsp;Burak Un,&nbsp;Isabella Hetherington,&nbsp;Md. Abu Rahat,&nbsp;Marian Kacerovsky,&nbsp;Charles J. Lockwood,&nbsp;Ozlem Guzeloglu-Kayisli,&nbsp;Hana Totary-Jain","doi":"10.1111/aji.70310","DOIUrl":"https://doi.org/10.1111/aji.70310","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Inflammation contributes to spontaneous preterm birth, yet mechanisms regulating trophoblast inflammatory responsiveness remain unclear. Interleukin-1 beta (IL1β) is a potent mediator of labor-associated inflammation, but the role of its accessory receptor, IL-1 receptor accessory protein (IL-1RAP), at the maternal-fetal interface is poorly understood.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>IL-1RAP expression and localization were assessed in preterm chorioamniotic membranes with or without intra-amniotic inflammation. Decidual regulation of trophoblast IL1RAP was evaluated in primary trophoblasts, and gain- and loss-of-function studies in HTR8/SV^neo cells tested its role in IL-1β-induced inflammatory signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p><i>IL1RAP</i> expression was increased in fetal membranes from inflammation-associated preterm labor and IL-1RAP localized prominently to extravillous trophoblasts. Decidual cell-conditioned media increased trophoblast <i>IL1RAP</i> expression. IL1RAP overexpression enhanced basal and IL-1β-induced expression of inflammatory mediators, including <i>TNF</i>, <i>IL1B</i>, <i>IL6</i>, and <i>CXCL8/IL8</i>, whereas <i>IL1RAP</i> silencing most consistently attenuated IL-1β-induced <i>TNF</i> expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These findings identify trophoblast IL-1RAP as an amplifier of IL-1β-mediated inflammatory signaling and support further investigation of IL-1RAP in inflammation-associated preterm birth.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148783987","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":"The Value of Platelet-Rich Plasma Treatment in Reproductive Disorders: An Umbrella Review","authors":"Guangyu Ma,&nbsp;Wanrong Huang,&nbsp;Xun Zeng,&nbsp;Lang Qin,&nbsp;Rui Gao,&nbsp;Jian Chen","doi":"10.1111/aji.70305","DOIUrl":"https://doi.org/10.1111/aji.70305","url":null,"abstract":"<div>\u0000 \u0000 <p>Platelet-rich plasma (PRP) is an autologous regenerative therapy investigated for improving endometrial receptivity, ovarian function, and reproductive outcomes. To address inconsistent findings across existing reviews, we conducted an umbrella review of systematic reviews and meta-analyses identified from PubMed, Embase, Web of Science, and the Cochrane Library, with evidence appraised using AMSTAR-2 and GRADE. Twenty-one reviews were included. In women with recurrent implantation failure, intrauterine PRP was associated with improved live birth, clinical pregnancy, and biochemical pregnancy rates. Similar benefits were observed in women with previous implantation failure and in assisted reproductive technology (ART) populations. PRP also modestly increased endometrial thickness and implantation rates. In women with thin endometrium or intrauterine adhesions, PRP improved pregnancy outcomes and reduced cycle cancellation, while miscarriage rates were largely unchanged. Intra-ovarian PRP improved ovarian reserve markers, hormone profiles, oocyte yield, and embryo quality in women with poor ovarian response, premature ovarian insufficiency, or diminished ovarian reserve, although effects on pregnancy and live birth were variable. Overall, PRP shows potential benefits, but the certainty of evidence ranged from very low to moderate due to heterogeneity and methodological limitations. High-quality randomized controlled trials are required to confirm efficacy and guide clinical practice.</p>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753505","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":"Special Issue on New Horizons in HIV and Reproductive Health Research","authors":"Charles R. Wira,&nbsp;Susan Cu-Uvin,&nbsp;Barbara L. Shacklett,&nbsp;Florian Hladik,&nbsp;Alan Landay","doi":"10.1111/aji.70307","DOIUrl":"https://doi.org/10.1111/aji.70307","url":null,"abstract":"","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753866","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":"Is the HLA System Really Involved in Implantation, Pregnancy, or Abortion of the Fetus?: Strengths, Weaknesses, and Controversial Points","authors":"Alicia Hita,&nbsp;Carmen Botella,&nbsp;José Antonio Galian,&nbsp;Rosana González-López,&nbsp;Marina Fernández-González,&nbsp;María José Alegría-Marcos,&nbsp;Rosa Moya-Quiles,&nbsp;Helios Martínez-Banaclocha,&nbsp;Manuel Muro-Pérez,&nbsp;Javier Muro,&nbsp;Alfredo Minguela,&nbsp;Isabel Legaz,&nbsp;Manuel Muro","doi":"10.1111/aji.70309","DOIUrl":"https://doi.org/10.1111/aji.70309","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problems</h3>\u0000 \u0000 <p>Pregnancy is a sensitizing event for human leukocyte antigen (HLA) alleles, as the fetus, acting as a semi-allograft, expresses maternal and paternal haplotypes in a codominant manner. Consequently, the mother may develop anti-HLA antibodies directed against the paternal haplotype. However, unlike in organ transplantation, this sensitization is not usually associated with fetal rejection in multiparous women, raising a central question in reproductive immunology: How is maternal-fetal tolerance achieved and maintained?</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>This review examines the influence of the HLA system on the immunological mechanisms underlying maternal–fetal tolerance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Accumulating evidence suggests that this phenomenon results from a complex network of cellular and molecular interactions. The roles of non-classical HLA molecules, particularly HLA-G, the modulation of NK activity via KIR receptors, and the expansion of regulatory T cells, which contribute to the maintenance of systemic immunological tolerance, are highlighted. In parallel, the relevance of anti-HLA antibodies and polymorphisms in HLA regulatory regions in susceptibility to gestational complications has been investigated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>It considers how insights from reproductive immunology may inform related fields such as transplantation and oncology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753506","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":"Association Between Leukocytospermia and Varicocele in Patients With Infertility","authors":"Eslam M. Eldamnhoury,&nbsp;Ahmed I. El-Sakka","doi":"10.1111/aji.70308","DOIUrl":"https://doi.org/10.1111/aji.70308","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Male infertility is a complex condition affected by multiple anatomical, physiological, and biochemical factors. Among the most commonly risk factors are leukocytospermia and varicocele, which are associated with increased oxidative stress and affected sperm function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The aim of this study is to address the association between leukocytospermia and varicocele in patients with infertility.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We had revised the studies from 2000–2025 that addressed the role of each leukocytospermia, varicocele and both of them on infertility.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Recent studies have suggested a potential link between leukocytospermia and varicocele, particularly in infertile patients, with each condition potentially exacerbating the detrimental effects of the other.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This review had explored the independent and combined impacts of leukocytospermia and varicocele on semen parameters and hormonal profiles, shedding light on their roles in male infertility and underlining the importance of integrated diagnostic and therapeutic approaches.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148754093","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":"MiR-29c-3p Impairs the Adhesion of Endometrial Epithelial Cells via COL4A1/β-catenin in Endometriosis","authors":"Chengyuan Li,&nbsp;Jian Li,&nbsp;Xin Li,&nbsp;Lan Geng,&nbsp;Qiuju Zhang,&nbsp;Zhenhui Hou,&nbsp;Xi Xia","doi":"10.1111/aji.70291","DOIUrl":"10.1111/aji.70291","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Defective endometrial receptivity is an indispensable cause of infertility in endometriosis, yet the post-transcriptional regulatory mechanisms underlying this impairment remain poorly understood. The goal of this research was to describe how miR-29c-3p and its target, COL4A1, regulate endometrial epithelial cell function and embryo adhesion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Endometrial epithelial cells were obtained from 14 women (including 7 with endometriosis and 7 controls) undergoing in vitro fertilization (IVF). Expression levels of miR-29c-3p and COL4A1 were quantified. Gain- and loss-of-function tests were employed in Ishikawa cells to assess cell adhesion capabilities and delineate downstream signaling pathways implicated in implantation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Women with endometriosis had considerably higher levels of miR-29c-3p expression in their endometrial epithelium. Mechanistically, increased expression of miR-29c-3p suppressed COL4A1, downregulated E-cadherin, and impaired JAr spheroid attachment. Notably, COL4A1 knockdown recapitulated these phenotypes by encouraging epithelial-mesenchymal transition (EMT), thereby compromising adhesive capacity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings identify the miR-29c-3p/COL4A1/<i>β</i>-catenin axis as a pivotal hub controlling endometrial epithelial adhesion. In patients with endometriosis, this axis could be a potential molecular candidate to enhance fertility outcomes and restore endometrial receptivity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70291","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148704981","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":"Maternal High Fat Diet and Acute Viral Mimic Exposure Impact Placental Inflammation, Lipid Peroxidation and Cellular Proliferation-to-Death Ratio Across Mouse Pregnancy","authors":"Thaina Ferraz,&nbsp;Lucas Cardoso,&nbsp;Sadra Mohammadkhani,&nbsp;Enrrico Bloise,&nbsp;Kristin L. Connor","doi":"10.1111/aji.70290","DOIUrl":"10.1111/aji.70290","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Maternal obesity and viral infection induce placental inflammation, but how their co-exposure influence fetoplacental development remains unclear. We hypothesised that maternal high fat (HF) diet and viral infection would independently induce placental inflammation and lipid peroxidation, reduce antioxidant defence, and cellular turnover. Further, HF diet would compromise placental capacity to adapt to infection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>Female C57BL/6J mice were fed a control (CON) or 62% HF diet six weeks before and throughout pregnancy and injected with poly(I:C) (viral mimic) or vehicle (VEH) 24 h before sacrifice at gestational days (GD) 12.5, 15.5, and 18.5 (<i>n</i> = 5–8/group/GD). Placental inflammasome (NLRP3), oxidative stress (4-HNE), antioxidant defence (GPx-4), and cellular proliferation-to-death ratio (Ki-67, Caspase-3) were assessed by immunohistochemistry, and mRNA expression of <i>Tlr3</i>, <i>Irf3</i>, <i>Tlr4</i>, <i>Tirap</i>, and <i>Il-1β</i> were measured by qPCR. Data were analysed by linear mixed models (<i>p</i> ≤ 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>At GD12.5, infection was associated with increased <i>Tlr3</i> mRNA and immunoreactive (ir)-4-HNE, and reduced ir-GPx-4 expression in the placental labyrinth zone (LZ). By GD15.5, HF diet was associated with increased ir-NLRP3 in both LZ and junctional zones (JZ). Exposure to infection alone and co-exposure to HF diet and infection further increased LZ ir-NLRP3. At GD18.5, HF diet was associated with increased <i>Tirap</i> and <i>Il-1β</i> mRNA expression, ir-4-HNE in the JZ and ir-Caspase-3 in the LZ.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Maternal HF diet and infection exert distinct effects on the placenta across gestation, suggesting that maternal overnutrition might reduce the placenta's capacity to handle adverse exposures, which may increase susceptibility to poor fetal outcomes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683184","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":"EVT-Derived Migrasomes Provide Mechanistic Insights Into Antiphospholipid Syndrome-Associated Recurrent Miscarriage","authors":"Di Wang,&nbsp;Yu Xie,&nbsp;Hongyuan Zhang,&nbsp;Tingting Dong,&nbsp;Xiaoyu Liu,&nbsp;Yilei Li,&nbsp;Yan Zhang,&nbsp;Xietong Wang,&nbsp;Qian Zhou","doi":"10.1111/aji.70272","DOIUrl":"https://doi.org/10.1111/aji.70272","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Recurrent miscarriage (RM) is a complex pregnancy-related disorder closely associated with impaired extravillous trophoblast (EVT). Antiphospholipid antibody syndrome (APS) is an autoimmune condition that contributes to adverse pregnancy outcomes, including RM. However, the mechanism by which APS induces RM remains largely unclear. Migrasomes, a newly identified type of extracellular vesicle generated during cell migration, may regulate cellular functions through the transfer of microRNAs (miRNAs). Increasing evidence has suggested that migrasomes play important roles in the female reproductive system, particularly in pregnancy-related disorders such as RM. This study aimed to explore the potential role and underlying mechanism of EVT-derived migrasomes in the pathogenesis of RM associated with APS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>First, EVT-derived migrasomes (EVTDMs) were isolated from an in vitro RM/APS model established in HTR-8/SVneo cells. Differentially expressed miRNAs in EVTDMs were identified by small RNA sequencing, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The predicted target gene of hsa-miR-206 was further validated using a dual-luciferase reporter assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results showed that migrasome markers were readily detected in EVTDMs derived from HTR-8/SVneo cells. An in vitro RM/APS model was established by co-incubation with anti-β2-glycoprotein I antibody (anti-β2-GPI Ab). Migrasome-like vesicles were identified by confocal microscopy and transmission electron microscopy. MiRNA profiling revealed that hsa-miR-206 was significantly upregulated in EVTDMs from the RM/APS group. Based on bioinformatic prediction and dual-luciferase reporter assays, IKBKB was identified as a direct binding target of hsa-miR-206.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In conclusion, HTR-8/SVneo cells were capable of generating migrasome-like vesicles, and anti-β2-GPI Ab treatment altered the miRNA cargo of EVTDMs. Among the differentially expressed miRNAs, hsa-miR-206 was markedly upregulated and was validated to bind directly to the 3′UTR of IKBKB, suggesting a potential role in posttranscriptional regulation. However, the downstream functional consequences of this interaction remain to be further elucidated.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148617158","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":"Altered Distribution of CD14+ Macrophages and Reduced ROS Activity in Preeclamptic Placentas","authors":"Luis Donis-Maturano,&nbsp;Judith Yenny Flores-Colque,&nbsp;Juana Calderon-Amador,&nbsp;Nidia Carolina Moreno-Corona,&nbsp;Oziel David Pérez-Luna,&nbsp;Orestes López-Ortega","doi":"10.1111/aji.70295","DOIUrl":"https://doi.org/10.1111/aji.70295","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Pregnancy requires a delicate balance between maternal immune tolerance and protective responses, with macrophages playing a pivotal role in placental development and immune regulation. Preeclampsia, a hypertensive disorder that affects 5%–8% of pregnancies, is associated with immune dysregulation, oxidative stress, and impaired placental remodeling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>In this study, we investigated the distribution of CD14⁺ and CD11b⁺ cells and the production of reactive oxygen species (ROS) in placental tissues from healthy pregnancies and preeclampsia cases, from areas near the umbilical cord and the delivery channel and divided into maternal, maternal/fetal and fetal zones, of each area.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Immunofluorescence analysis revealed that in healthy placentas, CD14⁺ macrophages were heterogeneously distributed with enrichment in the fetal section near the delivery channel, whereas in preeclamptic placentas these cells accumulated predominantly in the umbilical cord region. No significant differences were observed for CD11b⁺ cells, although a tendency toward increased numbers was noted in preeclamptic tissues. ROS analysis showed no statistically significant changes, but preeclamptic placentas exhibited weaker fluorescence intensity, indicating reduced ROS activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that altered CD14⁺ and CD11b⁺ cells localization, together with diminished ROS signaling, may contribute to the pathophysiology of preeclampsia by impairing immune regulation and placental vascular remodeling.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"96 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70295","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148617157","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}