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

CONCLUSION: USP25 plays a crucial role in mitigating renal histopathological and functional damage during anti-GBM GN in mice. This protective effect is primarily attributed to USP25's ability to inhibit the differentiation of naïve CD4+ T cells into Th17 cells. The underlying mechanism may involve the downregulation of RORγt. Additionally, during increased inflammatory responses or Th17 cell differentiation, USP25 expression is activated, forming a negative feedback regulatory loop that attenuates immune activation.PMID:38616174 | DOI:10.1080/0886022X.2024.2338932
Source: Renal Failure - Category: Urology & Nephrology Authors: Source Type: research