USP25 attenuates anti-GBM nephritis in mice by negative feedback regulation of Th17 cell differentiation.

ABSTRACT:

Purpose

This study aimed to elucidate the role of USP25 in a mouse model of anti-glomerular basement membrane glomerulonephritis (anti-GBM GN).

Methods

USP25-deficient anti-GBM GN mice were generated, and their nephritis progression was monitored. Naïve CD4+ T cells were isolated from spleen lymphocytes and stimulated to differentiate into Th1, Th2, and Th17 cells. This approach was used to investigate the impact of USP25 on CD4+ T lymphocyte differentiation in vitro. Furthermore, changes in USP25 expression were monitored during Th17 differentiation, both in vivo and in vitro.

Results

USP25-/- mice with anti-GBM GN exhibited accelerated renal function deterioration, increased infiltration of Th1 and Th17 cells, and elevated RORγt transcription. <

SUBMITTER: Xu R 

PROVIDER: S-EPMC11018034 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature