ORIGINAL RESEARCH article
Front. Immunol.
Sec. Comparative Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1623613
Depletion of Myeloid-derived Suppressor Cells Alleviates Kidney Damage in Murine Membranous Nephropathy
Provisionally accepted
- 1Department of Clinical Laboratory, The Second Hospital of Jilin University, Changchun, Jilin, China, Changchun, China
- 2Institute of Frontier Medical Sciences, Jilin University, Changchun, China, Changchun, China
- 3Central Laboratory, The First Hospital of Jilin University, Changchun, Jilin, China, Changchun, China
- 4Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China., Changchun, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Based on previous studies on myeloid-derived suppressor cells (MDSCs) and T helper 17 (Th17) cells in patients with primary membranous nephropathy (PMN), we successfully established a murine PMN model to investigate the relationship between MDSCs, T cells, and disease progression. Our study demonstrated that MDSCs and their subclasses, as well as Th17 and T helper 2 (Th2) immune responses, were enhanced. In contrast, the proportion of T helper 1 (Th1) and regulatory T (Treg) cells decreased with PMN progression. Depletion of MDSCs with gemcitabine reduced the proportion of Th17 and Th2 cells and the expression of related transcription factors. Conversely, the proportions of Th1 and Treg cells increased in the circulation, spleen, lymph nodes, and kidneys, alleviating the clinical manifestations and pathological damage to the renal tissue in PMN model mice. These findings suggest that MDSCs, along with Th17 and Th2 responses, play critical roles in PMN progression. MDSCs may contribute to disease progression by regulating the differentiation and immune response of T-cell subclasses. The data provide new insights into the etiology, pathogenesis, clinical diagnosis, and treatment of membranous nephropathy.
Keywords: murine primary membranous nephropathy model, myeloid-derived suppressor cells, T helper 2, T helper 17, Regulatory T
Received: 06 May 2025; Accepted: 08 Aug 2025.
Copyright: © 2025 Li, Wei, Ma, Yang, Xiao, Liu and Teng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Anhui Wei, Institute of Frontier Medical Sciences, Jilin University, Changchun, China, Changchun, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.