ArticleNature communications2025
Chronic inflammation drives epididymal tertiary lymphoid structure formation and autoimmune fertility disorders in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Analysis of research hotspots and trends in epididymitis from 2014 to 2025: a visual analysis based on bibliometrics and scientific graphs from multiple databases.Frontiers in medicine · 2026Pooled it
- Immunological dynamics of the epididymis: from experimental insights to clinical translation.Reproduction & fertility · 2026Review
- SARS-CoV-2 triggers an NF-kB-driven proliferative response in epididymal clear cells of K18-hACE2 mice.Reproduction & fertility · 2026Article
- Depletion of CX3CR1Mucosal immunology · 2026Article
- Oxidative Stress and Inflammatory Biomarkers in Male Infertility: A Narrative Review of Diagnostic Value and Clinical Integration.Diagnostics (Basel, Switzerland) · 2026Review
- Male Infertility: A Comprehensive Review of Urological Causes and Contemporary Management.Journal of clinical medicine · 2026Review
- Immunological mechanisms and precision stratification in male infertility: from testicular immune privilege and danger signal amplification to seminal immune biomarkers and mechanism-tailored intervention.Frontiers in immunology · 2026Review
- Tertiary lymphoid structures in genitourinary cancers: a comprehensive review.Frontiers in oncology · 2026Review
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Proton-Secreting Cells as Drivers of Inflammation and Sperm Dysfunction in LPS-Induced Epididymitis.Function (Oxford, England) · 2025Article
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11 authors.
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Abstract
Gaps in knowledge about the epididymal mucosa contribute to the prevalent classification of male idiopathic infertility. Inflammatory triggers, such as infections and autoimmunity, can breach immune privilege, induce anti-sperm antibody (ASA) production, and impair fertility. However, the mechanisms governing ASA production are poorly characterized. Here, using a murine model of epididymitis induced by regulatory T cell (Treg) depletion, we show that the disruption of immunotolerance leads to chronic autoimmunity characterized by the presence of ASA, and distinct testicular and epididymal immune landscapes. These inflammatory features impair sperm function, contribute to epididymal damage, and drive subfertility. Treg depletion induces the formation of tertiary lymphoid structures (TLS) within the epididymis, as indicated by the presence of B and T cell clusters, fibroblasts, and high endothelial venules. Similar autoantibody responses were detected in the seminal plasma of infertile patients, suggesting conserved mechanisms. Thus, we provide an in-depth analysis of immune cell dynamics and TLS during epididymitis, offering insights for the development of precision-targeted therapies for fertility disorders, as well as the identification of new contraceptive strategies.
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