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Subject Area

Microbiology

Article Type

Original Study

Abstract

Objective The objective of the study was to assess the role of regulatory T cells (Tregs) in type 2 diabetic nephropathy (DN), particularly the contribution of Tregs to the degree of albuminuria as a marker of renal damage. Background Treg cells have immunoregulatory roles that might be involved in the pathogenesis of DN. Self-tolerance and allogeneic tolerance are mediated by Treg cells, and expression of this category of lymphocytes may be supposed to mediate the development of type 2 DN. Patients and methods We conducted a cross-sectional study on 45 patients with type 2 diabetes mellitus who were classified into three groups according to the degree of albuminuria, with group I representing normoalbuminuric patients, group II representing patients with moderately increased albuminuria (microalbuminuria), and group III representing patients with severely increased albuminuria (macroalbuminuria). Demographic data were recorded. Blood samples for laboratory variables were collected and measured using the standard methods. Flow cytometry analysis was used to assess the expression of Treg cells in the peripheral blood samples obtained from the three groups. Results CD4+CD25+Foxp3+ Treg cells expression in peripheral blood by flow cytometry analysis was significantly decreased among microalbuminuric patients when compared with normoalbuminuric patients and also macroalbuminuric patients showed a significant lowered expression of CD4+CD25+Foxp3+ Treg cells when compared with normoalbuminuric patients. There were statistically significant correlations between the median of Treg/lymphocyte percent and the following parameters: urinary albumin–creatinine ratio, duration of diabetes mellitus, and glomerular filtration rate among the three studied groups. Multivariate analysis showed that only Treg percent was an independent predictor of albuminuria (P = 0.046). Conclusion The results of this study suggest that Tregs might have a correlation with diabetic kidney disease development.

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