ArticleInternational journal of biological sciences2023
Rapamycin and Low-dose IL-2 Mediate an Immunosuppressive Microenvironment to Inhibit Benign Prostatic Hyperplasia.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 6 citations in OpenAlex.
- Macrophage pyroptosis drives luminal senescence and club-cell reprogramming in 5α-reductase inhibitor-treated prostatic hyperplasia.Experimental & molecular medicine · 2026Article
- T cell-derived CCL5 drives macrophage immunometabolic remodeling in chronic prostatitis via the CCR5-ERK-PKM2/HIF-1α axis.Redox biology · 2026Article
- Global stagnation and misaligned priorities in BPH drug development: a 25-year landscape analysis of clinical trial registries.npj aging · 2026Article
- Microbial Genomic Consortia in Prostate Cancer: Mechanistic Signaling, the Gut-Prostate Axis, and Translational Perspectives.Cancers · 2026Review
- Decoding benign prostatic hyperplasia at single-cell resolution: heterogeneity, inflammation, and beyond androgen-driven pathogenesis.Frontiers in immunology · 2026Review
- Nanomedicine for Benign Prostatic Hyperplasia: Pathological Axes and Translational Evidence.International journal of nanomedicine · 2026Review
- Beyond size: A comprehensive overview of small-volume benign prostatic hyperplasia.Current urology · 2025Review
- Plasma metabolites as mediators in the relationship between inflammation-related proteins and benign prostatic hyperplasia: insights from mendelian randomization.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benign prostatic hyperplasia (BPH) is a condition that becomes more common with age and manifests itself primarily as the expansion of the prostate and surrounding tissues. However, to date, the etiology of BPH remains unclear. In this respect, we performed single-cell RNA sequencing of prostate transition zone tissues from elderly individuals with different prostate volumes to reveal their distinct tissue microenvironment. Ultimately, we demonstrated that a reduced Treg/CD4+ T-cell ratio in the large-volume prostate and a relatively activated immune microenvironment were present, characterized partially by increased expression levels of granzymes, which may promote vascular growth and profibrotic processes and further exacerbate BPH progression. Consistently, we observed that the prostate gland of patients taking immunosuppressive drugs usually remained at a smaller volume. Furthermore, in mouse models, we confirmed that both suppression of the immune system with rapamycin and induction of Treg proliferation with low doses of IL-2 therapy indeed prevented the progression of BPH. Taken together, our findings suggest that an activated immune microenvironment is necessary for prostate volume growth and that Tregs can reverse this immune activation state, thereby inhibiting the progression of BPH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.