Role of alteration in Treg/Th17 cells’ balance in nephropathic patients with Type 2 diabetes mellitus
Keywords:
Type 2 diabetes mellitus, Treg/Th17 cells, diabetic nephropathyAbstract
Introduction: In type 2 diabetes mellitus, the adaptive immune system drives systemic inflammation, promoting insulin resistance and related complications, such as diabetic nephropathy. Increased infiltration of activated T lymphocytes has been found in patients with diabetic nephropathy. T-cell influx and accumulation are the factors that aggravate diabetic nephropathy and link with glomerular filtration surface and albumin excretion. An appropriate balance between pro-inflammatory (T helper 17: Th17, and T helper 1: Th1) and anti-inflammatory (regulatory T cells: Tregs) subsets of T cells is critical to maintain homeostasis and avoid inflammatory disease. The aim of this study was to determine the balance between T helper 17 and regulatory T cells in type 2 diabetic patients who have diabetic nephropathy.
Methods: This case control study was conducted between December 2013 and June 2014 in Theodor Bilharz Research Institute in Egypt. Forty patients and 20 healthy volunteers were recruited in the study, and three groups were formed, i.e. two groups of cases with 20 patients in each group and one group of 20 controls) The groups were 1) 20 type 2 diabetic patients with nephropathy (group A); 2) 20 type 2 diabetic patients without nephropathy (group B); and 3) 20 healthy individuals (control group). Evaluation of T cells was done by standard 2-color flow cytometry.
Results: The study found higher mean of Th17 counts and Th17/Treg ratio among type 2 diabetic nephropathy patients compared to other groups; but a lower mean of Treg count was identified among type 2 diabetic nephropathy patients than in the other groups (p-value = 0.001).
Conclusion: The important role for regulatory T cells in the protection against nephropathy in type 2 diabetic patients was demonstrated, and also it was observed that T helper 17 cells were associated with renal affection.
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