514-P: Group 2 Innate Lymphoid Cells Promote Renal Fibrosis through the Production of Th2 Cytokines in Diabetic Kidney Disease
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 ty...
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Published in | Diabetes (New York, N.Y.) Vol. 68; no. Supplement_1 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
American Diabetes Association
01.06.2019
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Conference Proceeding-1 SourceType-Scholarly Journals-1 content type line 14 |
ISSN: | 0012-1797 1939-327X |
DOI: | 10.2337/db19-514-P |