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Abstract Generaly our study show statically higher level of t –regulatory cells in diabetic type 2 nephropathy compared to control healthy groups.. also our sudy show There was statistically significant difference between the two groups in hemoglobin level, eGFR. Also, in the current study type 2 diabetic nephropathy patients had statistically significant higher absolute Treg count, Treg/lymphocyte percentage than control; however, there was no statistically significant association between Treg variables and both duration of DM and proteinuria. Although scattered blot revealed statistically significant positive relation between Treg and serum creatinine and statistically significant inverse relation between Treg and eGFR; multivariate analysis showed that Treg count was an independent predictor of eGFR with a borderline statistical significance. In conclusion As regard these conflicting results about role of inflammatory cells in development of diabetic nephropathy, still conventional pathways for diabetic kidney disease has the superiority in explaining the development of diabetic kidney disease caused by at least renal hemodynamic changes, ischemia and glucose metabolism abnormalities- associated oxidative stress increases, inflammatory processes and overactive renin-angiotensin-aldosterone system (RAAS). In persistent hyperglycemia, AGEs and oxidized lipoproteins causes macrophage recruitment which then facilitates the recruitment of leukocytes and mast cells in the kidney. These immune responses accelerate renal damage and decline of renal function in DKD. Hence, the inflammation in DKD is involved in the activation of innate immune responses rather than adaptive immune responses postulated. |