ArticleJournal of advanced research2025
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.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury.Cell communication and signaling : CCS · 2026Article
- Homoharringtonine and Gilteritinib Synergistically Induce Apoptosis and Suppress Viability in FLT3-ITD-Positive AML Cells.Biomedicines · 2026Article
- Integrated single-cell and bulk transcriptomic analyses reveal cDC1-centered ubiquitination dysregulation and identify UBE2F as a critical regulator in sepsis.Frontiers in immunology · 2026Article
- Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDendritic 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.
methodsAn online available dataset and specimens collected from AKI patients were used to analyze FLT3L expression. Wild type (WT) mice, T cell-deficient (Tcra
resultsCirculating FLT3L levels were significantly elevated in patients with AKI. This correlated with the degree of kidney dysfunction observed in these patients. Flt3L was expressed in and released by tubular epithelial cells, with minimal expression in immune cells. Flt3L primarily promoted the activation and expansion of cDC1s and polarization of CD4
conclusionFlt3L is upregulated in both humans and mice during IRI-induced AKI and is likely produced by tubular epithelial cells. It mainly promotes the expansion and activation of kidney cDC1 cells, thereby reducing the severity of AKI in mice. These findings suggest that Flt3L-dependent, cDC1-targeted immunotherapy could be a promising strategy for treating AKI.
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