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.

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Tác giả: Yun Chen, Yao Guo, Mingcheng Huang, Shan Jiang, Muzheng Li, Na Li, Stefanie Steiger, Xiaohua Wang, Zheqi Wen, Chuyu Xie, Liuting Yu, Dengyang Zhang, Yuming Zhao, Zhizhuang Joe Zhao, Zhihua Zheng

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Egypt : Journal of advanced research , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 739409

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 RESULTS: Circulating 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 CONCLUSION: Flt3L 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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