ArticlePLoS pathogens2024
Interferon epsilon is produced in the testis and protects the male reproductive tract against virus infection, inflammation and damage.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Age-dependent expression and antiviral activity of interferon epsilon in respiratory epithelium.Journal of virology · 2026Article
- Article
- Epidemiological and pathogen characteristics of symptomatic male reproductive tract infections in Hunan province: retrospective study.Scientific reports · 2026Article
- Striking the right balance with type I interferon signalling in cancer.Nature reviews. Cancer · 2026Review
- Article
- Immunological dynamics of the epididymis: from experimental insights to clinical translation.Reproduction & fertility · 2026Review
- Advances in immunological research on male infertility.Frontiers in reproductive health · 2026Review
- Human interferon-ω: an underappreciated type I interferon.Frontiers in immunology · 2026Review
- Decoding the Puzzle of Male Infertility: The Role of Infection, Inflammation, and Autoimmunity.Diagnostics (Basel, Switzerland) · 2025Review
- Macrophage TRIM21 lactylation exacerbates infection-induced orchitis through enhancing STAT1-mediated CXCL9 and CXCL10 production.Frontiers in immunology · 2025Article
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The testis is a reservoir for viruses that can cause persistent infection and adversely affect male reproductive health, an observation commonly attributed to deficiencies in inducible antiviral defence mechanisms. In this study, we demonstrate that interferon-epsilon (IFNε), a type I interferon initially discovered in female reproductive epithelia, is constitutively expressed by meiotic and post-meiotic spermatogenic cells, Leydig cells and macrophages in mouse testes. A similar distribution pattern was observed in human testes. Mice lacking IFNɛ were more susceptible to Zika virus-induced inflammation and damage of the testis and epididymis compared to wild-type mice. Exogenous IFNε treatment reduced the viral infection burden in cultured human testicular cells by inducing interferon-stimulated gene expression, and reducing inflammatory gene expression and cell damage. Treatment was more effective when administered prior to infection. These data indicate a critical role for constitutively-expressed IFNɛ in limiting viral infection and inflammatory damage in the male reproductive tract.
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