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Abstract

Abstract Title

CD4+ T cells eliminate senescent prostate epithelium to delay progression of benign prostatic hyperplasia

Presentation Type

Podium Abstract

Manuscript Type

Basic Research

Abstract Category *

Benign Prostate Hyperplasia and Male Lower Urinary Tract Symptoms: Medical Treatment

Author's Information

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Co-author 1

Li Senmao msli612@163.com The Second Affiliated Hospital of Kunming Medical University Department of Urology Kunming China *

Co-author 2

Ding Mingxia Dmx7166@126.com The Second Affiliated Hospital of Kunming Medical University Department of Urology Kunming China

Co-author 3

Wang Haifeng wanghaifeng@kmmu.edu.cn The Second Affiliated Hospital of Kunming Medical University Department of Urology Kungming China

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Abstract Content

Introduction

Benign prostatic hyperplasia (BPH) is an age-related condition marked by progressive prostate enlargement. The accumulation of senescent cells and their senescence associated secretory phenotype (SASP) are critical drivers of BPH progression.

Materials and Methods

We tested the cellular senescence and SASPs of BPH tissues through single-cell RNA sequencing and laser capture microdissection, Immunohistochemistry and functional assays confirmed that senescent cells release SASPs, and in a testosterone-induced BPH mouse model in vivo for further experimental verification.

Results

Through single-cell RNA sequencing and laser capture microdissection of BPH tissues,we identified C-X-C motif chemokine ligand 13 (CXCL13) as a key chemokine recruiting CD4+ T cells to senescent prostate epithelial cells. Immunohistochemistry and functional assays confirmed that senescent cells release CXCL13, attracting CD4+T cells via CXCR5, which engage senescent cells through HLA-DR to facilitate their clearance, potentially attenuating BPH. In a testosterone-induced BPH mouse model,treatments with recombinant CXCL13 and anti-CD4 antibodies supported this mechanism, corroborated by murine single-cell data.

Conclusions

This study reveals immune regulation of senescent cells in BPH and highlights CXCL13-mediated CD4+ T cell recruitment as a promising therapeutic target for age-related prostate enlargement.

Keywords

single-cell; cellular senescence; CD4+ T; CXCL13; BPH.

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