Tubular epithelial cell-derived Flt3L is required for type 1 conventional dendritic cell (cDC1) activation and expansion in promoting the recovery in acute kidney injury.

ABSTRACT:

Introduction

Dendritic cells (DCs) play a crucial role in the recovery following acute kidney injury (AKI). Fms-related tyrosine kinase 3 ligand (Flt3L) is essential for the generation and maintenance of DCs. However, the cellular source of Flt3L in the kidney and its contribution on renal DC function during AKI remain unclear.

Methods

An online available dataset and specimens collected from AKI patients were used to analyze FLT3L expression. Wild type (WT) mice, T cell-deficient (Tcra^KO), and type 1 conventional DC (cDC1)-deficient (Irf8^KO) mice underwent ischemia-reperfusion (IR) injury to induce AKI. These mice were treated with either mouse recombinant Flt3L (rFlt3L) or the Flt3 inhibitor gilteritinib. In vitro experiments with human and murine bone

SUBMITTER: Li N 

PROVIDER: S-EPMC12684932 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature