Aim: To explore the role of Group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD).

Methods: The proportion of ILC2s and ILC2s-producted Th2 cytokines (IL-4, IL-5, IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed using flow cytometry and ELISA. Renal tubular epithelial cells (HK-2) were stimulated with IL-4 or IL-13 in the presence or absence of high glucose and the expression and release of transforming growth factor-β1 (TGF-β1) and fibronectin (FN) was analyzed using qPCR and ELISA.

Results: The proportion of ILC2s and the level of IL-4, IL-5, and IL-13 were significantly increased with the severity of DKD (P<0.05). The expression and release of TGF-β1 and FN were significantly upregulated by IL-4 or IL-13 in HK-2 cells (P<0.05). Compared with high glucose stimulation alone, treatment with IL-4 or IL-13 combined with high glucose significantly stimulated HK-2 cells to increase expression of FN and TGF-β1 (P<0.05).

Conclusions: ILC2s may promote the development and progression of diabetic kidney disease by secreting Th2 cytokines (IL-4 and IL-13) and promoting renal fibrosis.


C. Liu: None. L. Zhou: None. C. Gao: None. T. Zhang: None. M. Guo: None. W. Huang: None. Z. Jiang: None. J.Y. Ding: None. Y. Xu: None.

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