Journal of Reproductive Immunology最新文献

{"title":"Human uterine NK cells express CD96/TACTILE under the regulation of IL-15 and TGFβ1","authors":"Corinna Mayer ,&nbsp;Dan Sun ,&nbsp;Jonas Thier ,&nbsp;Benedikt Strunz ,&nbsp;Katharina Schott ,&nbsp;Helen Kaipe ,&nbsp;Vanessa Lundin ,&nbsp;Sebastian Gidlöf ,&nbsp;Niklas K. Björkström ,&nbsp;Martin A. Ivarsson","doi":"10.1016/j.jri.2025.104647","DOIUrl":"10.1016/j.jri.2025.104647","url":null,"abstract":"<div><div>Uterine natural killer (uNK) cells are a tissue-specific subset of innate lymphocytes with unique functions including the engagement with placenta-derived extra-villous trophoblast (EVT) cells. While several receptor-ligand pairs of this interaction have been identified, many remain poorly characterized. Here, we investigated the expression and regulation of nectin-like receptor CD96/TACTILE on human uNK cells, which recognizes ligands expressed by EVT cells. Using flow cytometry, we analysed NK cells from menstrual blood and from first- and second-trimester decidua, alongside peripheral blood cells used as reference. We identified a predominant exon 4-lacking splice variant of CD96 on uNK cells and found that CD96 is part of a broader set of receptors associated with NK cell tissue-residency regulated by IL-15 and TGFβ1. In vitro, IL-15 and canonical as well as non-canonical TGFβ1 signalling upregulate CD96 surface expression. Finally, redirected cross-linking assays showed no major effect of CD96 engagement on degranulation in decidual NK (dNK) cells. Taken together, these findings reveal that human uNK cells adapt to an IL-15- and TGFβ1-rich environment by shifting nectin-like receptor expression, with potential implications for dNK–EVT interactions during placentation.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104647"},"PeriodicalIF":2.9,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080984","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":"Linking altered gut microbiome to polycystic ovarian syndrome through immune mediated pathway","authors":"Vaishnavi A. Pathak ,&nbsp;Sanjay J. Kshirsagar ,&nbsp;Gitanjali S. Deokar","doi":"10.1016/j.jri.2025.104648","DOIUrl":"10.1016/j.jri.2025.104648","url":null,"abstract":"<div><div>Polycystic ovarian syndrome (PCOS) is an endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and metabolic disturbances. A balanced gut microbiome plays an important role in managing homeostatic signalling pathways in the body. These pathways regulate normal bodily functions but can become dysregulated under dysbiotic conditions. Recent research has highlighted the role of gut microbiota in the pathogenesis of polycystic ovarian syndrome. Key Bacterial taxa such as <em>Akkermansia, Prevotella, Lactobacillus, Escherichia coli, Bacteroides</em> and <em>Ruminococcaceae</em> (family-level) whose abundance is correlated with disease severity. At dysbiotic conditions, the pathobionts bypass the tight gut junction, enters the systemic circulation and trigger an immunomodulatory response subsequently releasing proinflammatory cytokines. Initially, first line and second line defence mechanisms are generated through immune responses such as IgG-mediated mechanisms. The immunological responses and inflammation cause macrophage pyroptosis, hormonal imbalance, and polycystic ovaries, followed by insulin resistance and hyperinsulinemia. Also, neuroendocrine alterations including dysregulation of GnRH secretion is influenced by gut-derived metabolites. The current review aids in understanding the mechanism pathway between gut microbiota and polycystic ovaries. Understanding ‘The Gut-PCOS axis’ explores various ways for targeting gut microbiota through prebiotics, probiotics and synbiotics as a potential therapeutic approach for polycystic ovarian syndrome management.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104648"},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145047035","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":"Postpartum levels of circulating fetal microchimeric cells are lower after early-onset preeclampsia","authors":"Daniel P. Jacobsen ,&nbsp;Heidi E. Fjeldstad ,&nbsp;Maria B. Olsen ,&nbsp;Meryam Sugulle ,&nbsp;Therese Schjørlien ,&nbsp;Mona Skjelland ,&nbsp;Bente Halvorsen ,&nbsp;Anne Cathrine Staff","doi":"10.1016/j.jri.2025.104646","DOIUrl":"10.1016/j.jri.2025.104646","url":null,"abstract":"<div><div>Fetal cells may persist in the mother following pregnancy, termed fetal microchimerism. These cells have been attributed positive and negative effects. The number of fetal cells transferred during pregnancy appears to be higher in preeclampsia. Here, we investigate whether fetal cell presence and quantity in the maternal circulation 1–8 years postpartum is influenced by a previous preeclamptic pregnancy. We also relate fetal cells detected postpartum to fetal cells detected during pregnancy, time since index pregnancy, parity, fetal sex and maternal characteristics. A cohort of 139 women was included in the present study: 21 with previous early-onset preeclampsia, 31 with previous late-onset preeclampsia and 87 with a clinically uncomplicated index pregnancy. Circulating fetal microchimerism was detected in maternal buffy coat using qPCR, targeting alleles unique to the fetus. Pregnancy buffy coat samples were available for 129 of the 139 included women. Early-onset, but not late-onset, preeclampsia was associated with reduced quantity of fetal microchimeric cells in maternal circulation postpartum. Fetal cells detected during pregnancy, time since index pregnancy, parity, fetal sex and maternal characteristics were not predictive of microchimerism postpartum in our cohort. Our findings suggest that early-onset, but not late-onset preeclampsia, affects circulating microchimerism postpartum. Our observation that fetal microchimerism postpartum did not correlate with number of fetal cells detected during pregnancy nor time since index pregnancy supports the notion that fetal microchimerism is a dynamic phenomenon, with fetal cells moving in and out of maternal circulation and surrounding tissues, possibly affected by the current physiologic state of the mother.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104646"},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145060870","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":"A 2025-update of “historical evolution of ideas on eclampsia/preeclampsia’’ (2017, workshop reunion 2016)","authors":"Pierre-Yves Robillard ,&nbsp;Nandor G. Than ,&nbsp;Silvia Iacobelli ,&nbsp;Francesco Bonsante ,&nbsp;Malik Boukerrou ,&nbsp;Marco Scioscia ,&nbsp;Phuong Lien Tran ,&nbsp;Gustaaf Dekker","doi":"10.1016/j.jri.2025.104639","DOIUrl":"10.1016/j.jri.2025.104639","url":null,"abstract":"<div><div>This paper updates the 2017 article, “Historical Evolution of Ideas on clampsia/Preeclampsia: A Proposed Optimistic View of Preeclampsia”, published in the Journal of Reproductive Immunology, incorporating advances in preeclampsia research from 2017 to 2025. Eclampsia, documented for over 5000 years, remains a critical challenge in maternal-fetal medicine. We outline the historical progression of understanding preeclampsia, from early observations of proteinuria and hypertension to modern molecular insights. Key advancements include recognizing preeclampsia as a systemic endothelial disorder, the primipaternity concept, and distinguishing early-onset (EOP) and late-onset (LOP) preeclampsia. A 2024 study reaffirms primipaternity as a major risk factor, resolving a 22-year debate over birth intervals. We explore inositol phosphoglycans P-type (IPG-P) as a specific biomarker, antiangiogenic factors like sFlt-1, and proteomic subclassifications identifying four molecular subtypes. Additionally, 75 % of fetal growth restriction (FGR, i.e. known pathological ultrasound Doppler) cases occur without maternal preeclampsia, suggesting an evolutionary protective mechanism. Despite progress, affordable treatments remain elusive, particularly for low-income countries. Targeting IPG-P, pravastatin, or ergothioneine, and leveraging proteomic insights, could lead to breakthroughs in preeclampsia prevention and treatment, potentially resolving related conditions like FGR and preterm birth.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104639"},"PeriodicalIF":2.9,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145027365","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":"RLR pathways in pregnancy: Guardians of antiviral immunity and mediators of inflammation-driven complications","authors":"Ayushi Vaidhya ,&nbsp;G. Ravi Prakash ,&nbsp;V. Deepthi ,&nbsp;Laxmi Singh Rathore ,&nbsp;Manjit Panigrahi ,&nbsp;V.A. Aneesha ,&nbsp;C.L. Madhu ,&nbsp;T.U. Singh ,&nbsp;Subhashree Parida","doi":"10.1016/j.jri.2025.104637","DOIUrl":"10.1016/j.jri.2025.104637","url":null,"abstract":"<div><div>Pregnancy demands dynamic immune adaptations to support implantation, fetal growth, and labor while maintaining maternal-fetal tolerance. The immune profile shifts from pro-inflammatory during implantation to anti-inflammatory in mid-pregnancy, reverting to inflammation at labor onset. Key immune cells like NK cells, macrophages, dendritic cells, and T cells dominate the decidua, guiding successful placental development. These immune cells express pathogen recognition receptors (PRRs) such as Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs), and C-type lectin receptors (CLRs) at the maternal–fetal interface and detect pathogen-associated molecular patterns (PAMPs) during pathological conditions. Among them, RIG-I-like receptors (RLRs), including RIG-I and MDA5, are expressed in syncytiotrophoblasts and cytotrophoblasts, where they sense RNA viruses like Zika and dengue during pregnancy. RLR signalling in pregnancy is modulated by hormones like estrogen and glucocorticoids. Cellular metabolic product lactate also regulates this signalling. The RLR signaling pathway is crucial for antiviral defense at the maternal-fetal interface, but its dysregulation can lead to complications like preeclampsia and preterm birth. Therapeutic targeting of RLR components and interferon regulators offers promising treatment avenues. Diagnostic biomarkers like circulating RLR molecules may aid in early detection of pregnancy disorders. Overall, RLR signaling presents both therapeutic and diagnostic potential in managing inflammation-associated pregnancy complications.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104637"},"PeriodicalIF":2.9,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145020370","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":"Novel T cell receptor expression features in sperm and testis","authors":"Tania Antonopoulou,&nbsp;Theologia Morfoniou,&nbsp;Kiki Sarganaki,&nbsp;Vasileia Pateraki,&nbsp;Lamprini Nouli,&nbsp;Markela Antoniou,&nbsp;Irene Athanassakis","doi":"10.1016/j.jri.2025.104638","DOIUrl":"10.1016/j.jri.2025.104638","url":null,"abstract":"<div><div>Except from the myeloid in origin cells, ectopic expression of T-cell receptors (TCRs) was also detected in sperm and the female reproductive tract, which in conjunction with major histocompatibility complex (MHC) molecules suggested their involvement in mate choice. Following-up these observations and considering that MHC/TCR interactions could guide spermatozoa towards ovum, the present study aimed to delineate the presence of TCRs in sperm <em>vis-à-vis</em> cognate recognition and define such expression during spermatogenesis. Immunofluorescence experiments using fertile BALB/c males showed that despite the inbred origin of mice, all combinations of high (HI, &gt;20 % expression) and low (LO, &lt;5 % expression) TCRαβ and TCRγδ expression could be detected in equal distribution rates, followed by an inverse pattern of MHC expression. Samples TCRαβΗΙ did not express MHCI/II, but TCRαβLO/TCRγδHI samples showed increased expression of MHCII. High expression TCRαβ samples also expressed CD3e and CD4, but at lower than expected levels. In all cases, soluble TCRs and MHCs were detected by ELISA in the seminal fluid, where TCRαβ highly correlated with MHCI/II and TCRγδ with MHCI. Except from the classical α, β, γ and δ transcripts, RT-PCR experiments detected additional, not-yet identified products for α and γ genes. Fluorescent microscope analysis identified TCRαβ and TCRγδ expression in spermatozoa tail. Immunohistology and cell dissociation of testis also detected TCR expression during spermatogenesis. Apart from un-folding novel structural, functional and regulatory features of TCRs in non-T cells, the results favor the involvement of TCRs in male reproduction and could serve as diagnostic markers in unexplained infertility.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104638"},"PeriodicalIF":2.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145020369","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":"Risk factors for moderate/severe bronchopulmonary dysplasia: A retrospective cohort study including results of an accurate assessment of intra-uterine microbes","authors":"Mayuko Takeuchi ,&nbsp;Satoshi Yoneda ,&nbsp;Noriko Yoneda ,&nbsp;Masami Ito ,&nbsp;Kanto Shozu ,&nbsp;Tatsuhiro Tsuda ,&nbsp;Akitoshi Nakashima ,&nbsp;Taketoshi Yoshida ,&nbsp;Hideki Niimi ,&nbsp;Shigeru Saito","doi":"10.1016/j.jri.2025.104636","DOIUrl":"10.1016/j.jri.2025.104636","url":null,"abstract":"<div><div>A highly sensitive PCR method developed in our university accurately identifies the presence or absence of intra-uterine (IU) microbes without false positive results. With the inclusion of the results of an accurate assessment of IU microbes, risk factors for the development of moderate/severe bronchopulmonary dysplasia (BPD), a chronic lung disease that affects premature infants who require prolonged oxygen therapy or medical ventilation, were examined in 107 spontaneous preterm neonates. Perinatal risk factors were compared between cases of moderate/severe BPD (N = 49) and mild/non-BPD (N = 58). There were no cases of IU <em>Ureaplasma</em>/<em>Mycoplasma</em> infection alone. IU coinfections defined as mixed infections of <em>Ureaplasma</em>/<em>Mycoplasma</em> and other bacteria (bacteria other than <em>Ureaplasma</em>/<em>Mycoplasma</em>) (54.0 %), histological chorioamnionitis ≥II using Blanc’s classification showing a maternal inflammatory response with neutrophil inflammation extending deeper into the chorion and/or amnion (69.4 %), delivery weeks [26 (22 – 32) weeks], and male sex (65.3 %) in moderate/severe BPD cases significantly differed from those in mild/non-BPD cases [16.7 %, 46.5 %, 28 (23−32) weeks, and 44.8 %, respectively] (<em>p</em> &lt; 0.01, <em>p</em> = 0.01, <em>p</em> &lt; 0.01, and <em>p</em> = 0.03, respectively). IU coinfections [odds ratio (OR) 5.4, 95 % confidence interval (CI) 1.7 – 17.0, <em>p</em> &lt; 0.01], neonatal immaturity (OR 4.8, 95 % CI 1.6 – 14.3, <em>p</em> &lt; 0.01), and male sex (OR 3.3, 95 % CI 1.1 – 9.8, <em>p</em> = 0.03) were identified as independent risk factors for the development of moderate/severe BPD. IU coinfections, such as <em>Ureaplasma</em>/<em>Mycoplasma</em> and other bacteria, were associated with the development of moderate/severe BPD.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104636"},"PeriodicalIF":2.9,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989412","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":"David A. Clark (1943–2025)","authors":"Petra Clara Arck","doi":"10.1016/j.jri.2025.104635","DOIUrl":"10.1016/j.jri.2025.104635","url":null,"abstract":"","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"172 ","pages":"Article 104635"},"PeriodicalIF":2.9,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989410","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":"Intravenous immunoglobulin (IVIg) use in recurrent implantation failure: Is it time for another randomized controlled trial?","authors":"Genevieve Genest ,&nbsp;Zhiyang Liu ,&nbsp;Martine Boivin ,&nbsp;Fernando Alvarez ,&nbsp;Shorooq Banjar ,&nbsp;Shaonie Ton-leclerc ,&nbsp;Rabea Khoudja ,&nbsp;Einav Kadour Peero ,&nbsp;Ciriaco A. Piccirillo ,&nbsp;Bruce D. Mazer","doi":"10.1016/j.jri.2025.104634","DOIUrl":"10.1016/j.jri.2025.104634","url":null,"abstract":"<div><div>Recurrent implantation failure (RIF) affects up to 5 % of patients undergoing in-vitro fertilization (IVF) yet remains unexplained in over 50 % of cases. Perturbation of the permissive immune environment required for implantation is thought to explain a proportion of RIF cases but remains a diagnosis of exclusion due to the lack of validated testing to confirm the condition. Patients are often empirically treated with immunomodulatory medications, with intravenous immunoglobulin (IVIg) being prominently featured. While some suggest potential benefit, available studies are heterogenous, often underpowered and do not consider recent definitions of RIF; IVIg remains a heavily debated IVF adjunct. With the recent COVID pandemic-induced global blood product shortage, IVIg prescribing practices for RIF must be reviewed. A well designed, adequately powered randomized controlled trial (RCT) is needed to determine if IVIg should be featured in our armamentarium. However, prior to its design, data amassed over the last 3 decades must be incorporated to ensure it yields robust and clinically meaningful data. This narrative review synthesizes our current state of knowledge on the topic, discussing proposed mechanisms of immune-mediated RIF, potential mechanisms of action of IVIg as well as patient populations most likely to benefit from immune-modulation. Lastly, with use and prices of IVIg rising globally, we discuss our collective responsibility towards ensuring IVIg stewardship while proposing timely and cost-effective interventions for our patients.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"171 ","pages":"Article 104634"},"PeriodicalIF":2.9,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144890367","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":"Poly(I:C) stimulates cytokine production, but not cell migration, in an extravillous trophoblast cell line","authors":"B.C. Hameete ,&nbsp;A. Hogenkamp ,&nbsp;T. Plösch ,&nbsp;L. Groenink","doi":"10.1016/j.jri.2025.104632","DOIUrl":"10.1016/j.jri.2025.104632","url":null,"abstract":"<div><div>Extravillous trophoblasts play an important role during pregnancy due to their involvement in spiral artery remodeling and immune privilege. Extravillous trophoblast dysfunction is thus implicated in a variety of pregnancy complications, such as those arising after maternal immune activation caused by infection. The aim of this study was to improve our understanding of how viral infection might affect extravillous trophoblast functioning. In a randomized, blinded set-up, cells of the extravillous trophoblast cell line HTR8/SVneo were exposed to polyinosinic polycytidylic acid (poly(I:C)), a viral mimetic that acts as a toll-like receptor (TLR)-3 agonist. After exposure of the cells to poly(I:C) in concentrations up to 200 µg/ml, analyses were performed for cytotoxicity, interleukin(IL)-1β, IL-6, IL-8, RANTES, interferon-γ, tumor necrosis factor-α, human chorionic gonadotropin, progesterone, estradiol and cell migration. Exposure to poly(I:C) led to a significant increase in IL-6, IL-8 and RANTES concentrations in HTR8/SVneo cell culture supernatant, but did not significant affect concentrations of other cytokines included for measurement. Similarly, exposure to poly(I:C) did not affect hormone secretion or cellular migration. While poly(I:C) is capable of triggering the release of cytokines in HTR8/SVneo cells, the absence of an effect on migration suggests that the core function of extravillous trophoblasts might not be affected by TLR-3 stimulation. These results indirectly suggest that IL-6, IL-8 and RANTES do not affect migration either. Future research is recommended to include a wide variety of immunological triggers to better map which ones may be relevant to extravillous trophoblast dysfunction.</div></div>","PeriodicalId":16963,"journal":{"name":"Journal of Reproductive Immunology","volume":"171 ","pages":"Article 104632"},"PeriodicalIF":2.9,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879242","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}