These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Gal-9/Tim-3 signaling pathway activation suppresses the generation of Th17 cells and promotes the induction of Foxp3+ regulatory T cells in renal ischemia-reperfusion injury.
    Author: Wang Y, Feng T, Li H, Xiong Y, Tao Y.
    Journal: Mol Immunol; 2023 Apr; 156():136-147. PubMed ID: 36921488.
    Abstract:
    CD4+ T cells mediate the pathogenesis of renal ischemia-reperfusion injury (IRI). Emerging research suggests that a Th17/regulatory T cell (Treg) imbalance plays a pivotal role in the development of renal IRI. A recently identified negative checkpoint protein, T cell immunoglobulin domain and mucin domain family 3 (Tim-3), inhibits the immune response by binding to its ligand, galectin-9 (Gal-9). However, the role of the Gal-9/Tim-3 signaling pathway in the regulation of CD4+ T cell subsets in renal IRI remains unclear. In this study, we investigated the effect of the Gal-9/Tim-3 signaling pathway on Th17/Treg subsets in renal IRI using a mouse model. Renal IRI induced the expression of Gal-9 in renal tubular epithelial cells and increased the proportion of Tim-3+ Th17 cells and Tim-3+ forkhead box P3 (Foxp3)+ Treg cells in the ischemia-reperfusion (IR) kidneys. Administration of rAAV9-Gal-9 suppressed kidney inflammation, reduced the mortality of mice with renal IRI, increased Foxp3+ Treg cells, and reduced Th17 cells. In contrast, the blockade of Tim-3 in vivo using an anti-Tim-3 monoclonal antibody aggravated renal inflammation, decreased Foxp3+ Treg cells, and promoted Th17 cells. Thus, Gal-9/Tim-3 signaling pathway activation may protect against renal IRI by inhibiting Th17 cell production and inducing Foxp3+ Treg cell expansion. Our study suggests that the Gal-9/Tim-3 signaling pathway may be targeted by immunotherapy in renal IRI.
    [Abstract] [Full Text] [Related] [New Search]