JOURNAL OF REPRODUCTIVE IMMUNOLOGY生殖免疫学杂志
JOURNAL OF REPRODUCTIVE IMMUNOLOGY(英文缩写 J REPROD IMMUNOL),ISSN 0165-0378,eISSN 1872-7603,中文译名:生殖免疫学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.993 | Q2 |
| 2022 | 3.400 | Q2 |
| 2023 | 2.900 | Q2 |
| 2024 | 2.900 | Q2 |
| 2025 | 3.500 | Q1 |
JOURNAL OF REPRODUCTIVE IMMUNOLOGY 最新收录文献
-
1. Comparative analysis of immunocontraceptive vaccines in wild animals: Modes of action, molecular targets, and immunological responses.
1. 野生动物免疫避孕疫苗的比较分析：作用方式、分子靶点及免疫应答PMID:日期:2026-09-20Immunocontraceptive vaccines have emerged as a promising, non-invasive strategy for regulating fertility in wildlife, domestic animals, and humans, particularly in species such as elephants where conventional population control methods are often impractical or ethically challenging. These vaccines act by eliciting immune responses against critical reproductive targets, thereby disrupting gametogenesis, fertilization, or endocrine regulation. The major categories include gonadotropin-releasing hormone (GnRH)-based vaccines, zona pellucida (ZP)-based vaccines, and gamete-specific antigen vaccines. Anti-GnRH vaccines induce neutralizing antibodies that suppress the hypothalamic-pituitary-gonadal axis by inhibiting luteinizing hormone and follicle-stimulating hormone secretion, ultimately blocking steroidogenesis and gamete production. In contrast, ZP-based vaccines target oocyte surface glycoproteins, preventing sperm binding and fertilization. Emerging molecular targets, including sperm-egg interaction proteins such as IZUMO1 and JUNO, offer enhanced specificity. These vaccines predominantly stimulate humoral immune responses, with antigen-specific antibody production playing a central role, although cell-mediated immunity may contribute to sustained effects. In elephants, vaccines such as porcine zona pellucida (PZP) and GnRH-based formulations (e.g., GonaCon) have shown variable success in inducing reversible infertility, though challenges remain regarding booster requirements, duration of efficacy, and potential side effects. Advances in scientific technologies, particularly peptide engineering and viral-vector platforms, have contributed significantly to the development of immunocontraceptive vaccines by enhancing antigen specificity, immunogenicity, and overall vaccine performance. However, variability in immune responses, species-specific efficacy, and ethical considerations continue to limit widespread application. This review aims to help understanding the molecular and immunological mechanisms are essential for optimizing safe, effective, and sustainable fertility control strategies.
-
2. No broad PBMC cytokine-response fingerprint of endometriosis under PHA-stimulated culture conditions: A 27-plex case-control study.
2. 在PHA刺激培养条件下，子宫内膜异位症无广泛的PBMC细胞因子反应指纹特征：一项27重病例对照研究PMID:日期:2026-09-17Endometriosis is associated with immune dysregulation yet circulating cytokine measurements have shown limited discriminatory value. We investigated whether peripheral blood mononuclear cells (PBMCs) from women with endometriosis exhibit altered basal or phytohemagglutinin (PHA)-induced cytokine secretion. In this single-center case-control study, PBMCs from 36 women with laparoscopically and histopathologically confirmed endometriosis and 44 laparoscopy-confirmed controls without endometriosis were cultured for 24 h under unstimulated and PHA-stimulated conditions. Supernatant concentrations of 27 cytokines, chemokines and growth factors were measured using a Bio-Plex/Luminex assay. Cytokine concentrations were analyzed using linear mixed-effects models including group, condition, and group × condition interaction terms, with false-discovery-rate correction. PHA induced broad cytokine responses, with significant condition effects for 20 of 27 analytes in the full panel and 14 of 15 analytes in the robust quantifiable panel. A significant group × condition interaction was observed for IL-5; however, this result was based on very sparse PHA data and was not retained in a robust restricted panel of adequately quantified analytes. Exploratory multivariate analyses did not show clear group separation. Overall, these findings do not support the presence of a broad and reproducible endometriosis-associated cytokine-response profile in 24-h bulk-PBMC cultures stimulated with PHA-L at 5 µg/mL. Within this experimental framework, any between-group differences appeared subtle, analyte-specific, and sensitive to data completeness. These results are compatible with, but do not directly demonstrate, the concept that disease-related immune alterations may be more prominent in specific immune-cell subsets or local pelvic compartments than in non-specifically stimulated circulating PBMC cultures.
-
3. The impact of maternal gestational diabetes mellitus on the microbiome of offspring: A systematic review.
3. 母亲妊娠期糖尿病对子代微生物组的影响：一项系统性综述PMID:日期:2026-09-16Gestational diabetes mellitus (GDM) adversely affects maternal and offspring health, and the early-life microbiome is implicated in developmental programming. This systematic review quantitatively evaluated the association between maternal GDM and alterations in the gut and oral microbiomes of offspring. We systematically searched PubMed, Web of Science, and Embase (up to August 2025) for eligible studies adopting high-throughput sequencing techniques. Random-effects meta-analysis was performed for alpha diversity metrics, while findings on beta diversity and microbial taxonomy were summarized narratively. Twenty-one studies were included. The meta-analysis revealed no statistically significant differences in gut microbial alpha diversity between infants exposed to maternal GDM and unexposed controls. Beta diversity exhibited substantial inter‑study heterogeneity, with no consistent shifts observed. In infants born to mothers with GDM, several microbial taxa including Gammaproteobacteria, Enterobacteriaceae, Micrococcaceae, Propionibacteriaceae, Rikenellaceae, Megasphaera, Staphylococcus, Collinsella, Rothia, Pelomonas, Veillonella, Shewanellaceae and Prevotella tended to decrease in abundance, whereas Escherichia tended to increase. Notably, no microbial taxon presented consistent abundance changes in three or more studies, and these repeated findings were based on limited evidence. Delivery mode appeared to have minimal influence on offspring gut alpha diversity. Collectively, maternal GDM may not be strongly linked to shifts in offspring gut or oral microbial alpha diversity. However, the consistent dysregulation of specific microbial taxa in GDM-exposed offspring may exert potential impacts on offspring immune and metabolic development. Further longitudinal multicenter investigations are warranted to elucidate the causal relationships and long-term health implications of GDM-induced microbial alterations in children.
-
4. The local immune cell environment of uterine fibroids: a systematic review.
4. 子宫肌瘤的局部免疫细胞环境：一项系统综述PMID:日期:2026-09-13Uterine fibroids are benign tumours of the myometrium. For large and/or multiple fibroids, there are no fertility-sparing pharmacological therapies. Better understanding of fibroid pathophysiology is key to developing such treatments. Current understanding of the pathophysiology of fibroid development has largely centred on hormone dependent growth and regression. The uterus is highly immunologically active, and pathological lesions from other benign uterine conditions exhibit local differences in immune cell populations compared to neighbouring analogous tissue. Characterising the differences in the local immune cells between fibroid tissue and non-diseased myometrium will inform understanding of fibroid pathophysiology and future therapeutic targets. This systematic review synthesises current evidence on the immune cell presence within uterine fibroids. Existing studies suggest a trend towards increased macrophage infiltration in fibroid tissue compared to matched myometrium, and reduced macrophage presence following hormonal therapy. There are conflicting reports on fibroid leucocyte and mast cell populations. Only a limited number of studies investigated a broader panel of immune cells, including dendritic, natural killer and T cells. Considerable methodological heterogeneity was observed across studies, alongside a frequent lack of demographic reporting, and variable use of matched fibroid-adjacent and healthy myometrial controls. To better characterise the immunological environment of uterine fibroids and the hormonal mechanisms that may govern it, future studies should employ standardised methodology, comprehensive immune cell panels and larger sample sizes that are segregated by menstrual cycle phase.
-
5. {"_":"Inflammatory plasma transfer induces early ovarian CD8 accumulation without overt pathology.","sup":["+"]}
PMID:日期:2026-09-08Autoimmune-associated reproductive dysfunction is frequently linked to ovarian immune infiltration and circulating ovarian autoantibodies, yet it remains unclear whether circulating factors alone can initiate immune changes in the ovary before overt histopathology is detectable. In prior work using interferon-γ (IFN-γ) AU-rich element deletion (ARE) mice, chronic inflammation was associated with increased ovarian CD8 T cell infiltration and reproductive dysfunction. Here, we tested whether circulating factors from ARE mice are sufficient to induce early ovarian immune remodeling in healthy hosts. Pooled plasma from WT, ARE, or ARE female donors was administered intraperitoneally to age-matched WT female recipients, and tissues were harvested on day 8. Ovaries were assessed by H&E histopathology and CD8 immunohistochemistry; spleen and draining lymph nodes (dLNs) were analyzed by flow cytometry. In parallel, circulating anti-ovarian antibody levels were quantified in donors, and genotype-dependent ovarian tissue binding was evaluated by incubating Rag1 ovarian sections with donor plasma followed by immunofluorescent detection and whole slide image quantification. Passive plasma transfer did not induce overt ovarian histopathology by H&E at day 8. However, CD8 immunohistochemistry revealed a genotype-dependent increase in ovarian CD8 cell accumulation, highest in ARE plasma recipients. Moreover, flow cytometry showed increased CD8 T cell frequencies in dLNs in ARE plasma recipients. Donor ARE mice exhibited elevated circulating ovarian autoreactivity and their plasma showed increased binding to Rag1 ovarian tissue ex vivo. Together, these data indicate that short-term exposure to disease-associated plasma can initiate an ovarian immune shift.
-
6. TNF-α-driven immune imbalance in preeclampsia: The role of TNFR1/TNFR2 in monocyte subsets.
PMID:日期:2026-09-06Preeclampsia (PE) is a pregnancy-specific syndrome characterized by an intense systemic inflammatory response and monocyte activation, with increased production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α). Evaluation of TNF-α receptor expression (TNFR1 and TNFR2) in monocyte subpopulations may provide new insights into the inflammatory mechanisms underlying this syndrome. In this study, monocytes from 20 women with PE and 20 normotensive (NT) pregnant women were analyzed by flow cytometry for M1-like (TLR4, CD64) and M2-like (CD163, CD206) markers, as well as TNFR1 and TNFR2 expression. Plasma levels of TNF-α, interleukin (IL)-1β, transforming growth factor beta (TGF-β), IL-10; and the soluble forms of TNF-α receptors, sTNFR1 and sTNFR2, were measured by ELISA. Monocytes from women with PE exhibited increased expression of TLR4 and CD64 and reduced expression of CD163 and CD206 compared with the NT group. In addition, a higher percentage of both M1-like and M2-like monocytes expressing TNFR1 and TNFR2 were observed in PE. Plasma concentrations of TNF-α, IL-1β, TGF-β, and sTNFR1 were significantly increased, whereas IL-10 levels were reduced in women with PE. No significant differences were observed in sTNFR2 levels between groups. These findings indicate that PE is associated with a predominance of M1-like monocytes and a reduction in the M2-like phenotype, contributing to the systemic inflammatory state characteristic of the syndrome. This imbalance appears to be linked to enhanced activation of the TNF-α/TNFR1 axis and dysregulated TNFR2-mediated regulatory signaling, highlighting TNF-α-driven immune dysregulation as a potential contributor to PE pathophysiology.
-
7. The mechanism of autophagy in granulosa cells during the follicular development.
7. 卵泡发育过程中颗粒细胞自噬的机制PMID:日期:2026-09-02During follicular development, granulosa cell autophagy is dynamically involved in follicular growth, atresia, estrogen and progesterone synthesis, luteinization, and luteal regression. Granulosa cell autophagy is regulated by gonadotropins, estrogen, progesterone, oxidative stress, and multiple signaling pathways. Conversely, granulosa cell autophagy can also influence estrogen and progesterone synthesis by regulating lipid metabolism, mitochondrial quality control, and granulosa cell viability.However, the biological effects of autophagy are highly context-dependent. Moderate autophagy is an important mechanism for maintaining granulosa cell homeostasis and promoting follicular development, whereas excessive autophagy or impaired autophagic flux may lead to granulosa cell dysfunction, increased apoptosis, follicular atresia, and reproductive endocrine disorders. Dysregulated granulosa cell autophagy has been closely associated with ovulatory disorders such as polycystic ovary syndrome and premature ovarian insufficiency. Therefore, promoting follicular development through the regulation of autophagy may provide an important therapeutic entry point for ovulatory disorders. This review summarizes the roles and underlying mechanisms of granulosa cell autophagy in follicular development, follicular atresia, hormonal regulation, and ovulatory disorders, and proposes that maintaining autophagic homeostasis may represent a potential strategy for promoting follicular development and improving female reproductive health.
-
8. Aberrant integrin expression on peripheral blood NK cells of women with recurrent pregnancy losses and repeated implantation failures.
PMID:日期:2026-09-02Natural killer (NK) cells are key regulators of endometrial receptivity and placentation, and aberrant activation of peripheral blood NK (pNK) cells has been implicated in recurrent pregnancy loss (RPL) and repeated implantation failure (RIF). This study investigated adhesion molecule expression on pNK cells in women with primary RPL (pRPL), secondary RPL (sRPL), and unexplained infertility (uINF), and its associations with NK-cell phenotypes, cytotoxicity (NKC), and T-helper (Th)-1/Th2 (Th1/Th2) immune balance. Expression of adhesion markers LFA-1, VLA-1, VLA-2, and ICAM-1 on NK cells was assessed by flow cytometry. NKC was measured using the K562 assay, and Th1/Th2 cytokine ratios were determined by intracellular cytokine staining using flow cytometry. Total CD56⁺ NK cell proportions and overall NKC did not differ among groups. Expression of LFA-1, VLA-1, VLA-2, and ICAM-1 on total NK cells was also comparable. However, Th1/Th2 cytokine ratios were significantly lower in the sRPL group. Stratification by NKC revealed that women with RPL and higher NKC exhibited significantly increased ICAM-1 expression on cytotoxic subsets (CD56⁺CD16⁺ and CD56⁺CD57⁺). NKC positively correlated with ICAM-1-expressing NK subsets, while Th1/Th2 ratios were associated with mature and activated NK phenotypes in women with RPL. Although overall adhesion molecule expression did not differ by clinical classification, elevated ICAM-1 expression was associated with increased NKC and pro-inflammatory immune signatures in RPL but not in uINF, suggesting an association between ICAM-1 expression on NK cell subsets, increased NKC, and altered Th1/Th2 responses in RPL.
-
9. The role of lactate metabolism in uterine spiral artery remodelling.
PMID:日期:2026-08-27Lactate is a key metabolite of glycolysis. Since the proposal of the lactate shuttle hypothesis, accumulating evidence indicates that lactate is not only an essential energy substrate but also a key signalling molecule that regulates cellular functions under both physiological and pathological conditions. Uterine spiral artery (SpA) remodelling is a critical event in successful pregnancy. It involves complex interactions among trophoblasts, vascular smooth muscle cells (VSMCs), decidual immune cells, and endothelial cells (ECs). Similar to the tumour microenvironment, physiological hypoxia at the maternal-foetal interface during early pregnancy drives decidual cells, blastocysts, trophoblasts, and immune cells to undergo aerobic glycolysis, leading to local lactate accumulation and the formation of an acidic microenvironment. This review systematically elucidates the role and molecular mechanisms of lactate metabolism in SpA remodelling. It explores the association between dysregulated lactate metabolism and recurrent pregnancy loss (RPL), preeclampsia (PE), and foetal growth restriction (FGR). The findings of this review indicate that targeting lactate metabolism may represent a promising strategy for the management of pregnancy complications. Further in-depth mechanistic research and clinical obstetric research are warranted.
-
10. Ovarian microenvironment remodeling in premature ovarian insufficiency: From hormone replacement to regenerative strategies with mesenchymal stem cells and exosomes.
PMID:日期:2026-08-27Premature ovarian insufficiency (POI) is a heterogeneous disorder characterized by loss of ovarian function before age 40, causing infertility, hypoestrogenism-related complications, and significantly impaired quality of life. Although hormone replacement therapy (HRT) remains the standard treatment for symptom relief and long-term health protection, it cannot restore ovarian reserve or natural fertility. This review summarizes the etiology and pathogenesis of POI, emphasizing mitochondrial dysfunction, oxidative stress, chronic inflammation, and progressive deterioration of the ovarian microenvironment. We critically evaluate the strengths and limitations of conventional HRT based on the latest 2024 international evidence-based guidelines, and comprehensively overview emerging regenerative therapies, focusing on mesenchymal stem cells (MSCs) and MSC-derived small extracellular vesicles (sEVs). MSCs exert therapeutic effects mainly through paracrine actions, including anti-apoptotic, anti-inflammatory, and pro-angiogenic activities. MSC-sEVs, particularly hypoxia-preconditioned ones, offer a safer cell-free alternative. They protect mitochondrial function via the SIRT3/PGC-1α pathway and other related mechanisms such as Nrf2/Keap1 and AMPK signaling. Current clinical evidence for both approaches remains preliminary, consisting mainly of small-scale trials with heterogeneous protocols and short follow-up. We propose an innovative ovarian microenvironment remodeling framework that integrates symptomatic HRT with etiology-targeted regenerative interventions using MSCs or engineered sEVs. In summary, while HRT forms the foundation of POI management, MSC-sEVs represent a highly promising cell-free platform that may shift the paradigm from hormone replacement to functional regeneration, restoring both endocrine function and fertility in POI patients.