Activity of Group 2 Innate Lymphoid Cells is Associated with Chronic Inflammation and Dysregulated Metabolic Homoeostasis in Type 2 Diabetic Nephropathy

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Abstract

The metabolic syndrome (MS) is an independent risk factor for type 2 diabetic nephropathy and accompanied by subclinical inflammation which involves immune-deriving factors. Emerging studies indicate that group 2 innate lymphoid cells (ILC2s) can regulate adipose metabolism, but much less is known about the activity of ILC2s in metabolic imbalance in obesity and diabetes. This study explored the effect of ILC2s-related molecules on the occurrence of MS in type 2 diabetic nephropathy. Thirty patients with type 2 diabetic nephropathy were included in the study; the mRNA expression of ILC2s-associated molecules from peripheral blood mononuclear cell and the correlation of the ILC2s activity and the MS-related indicators were analysed. The results indicated that the waist circumference, fasting blood glucose, systolic blood pressure, diastolic blood pressure and triglyceride in patients with simple diabetes and diabetic nephropathy were increased, and the incidence of MS was 46.67% and 86.67%, respectively. The ILC2s-associated factors RORα, T1/ST2 and IL-5/IL-13 mRNA were increased in diabetic nephropathy. There was a positive correlation between the expression level of IL-13 or T1/ST2 mRNA and some MS indexes. In addition, the levels of plasma sTNFR, eotaxin-2 and I-309 were also increased in patients with type 2 diabetic nephropathy. It suggested that the patients with type 2 diabetic nephropathy were more likely to have multiple components of MS than those with simple type 2 diabetes mellitus, and enhanced ILC2s activity might be involved in the formation of MS in diabetic nephropathy via influencing blood pressure and lipid metabolism.

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Lu, P., Ji, X., Wan, J., & Xu, H. (2018). Activity of Group 2 Innate Lymphoid Cells is Associated with Chronic Inflammation and Dysregulated Metabolic Homoeostasis in Type 2 Diabetic Nephropathy. Scandinavian Journal of Immunology, 87(2), 99–107. https://doi.org/10.1111/sji.12637

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