الفهرس 
Diabetes MellitusOnly 14 pages are availabe for public view
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Abstract
Type 2 DM is a global health problem characterized by a defect in insulin secretion and/or a decrease in sensitivity to insulin. Obesity is recognized as a major contributor to insulin resistance.
Type 2 DM was historically considered a non-immune condition, in contrast to the well-established autoimmune etiology of Type 1 DM. But, recent work discovered that many immune mediators are implicated in causing chronic inflammation of the adipose tissue in Type 2 DM which in turn is responsible for the development and worsening of insulin resistance.
Adipose tissue is not a passive storage depot of fat, but can be considered as an endocrine gland, as it produces pro-inflammatory molecules which are implicated as active participants in the development of insulin resistance.
Treg cells, a small subset (5–20%) of T-lymphocytes, are thought to be one of the body’s most crucial defenses against inappropriate immune responses in autoimmunity, allergy, inflammation, infection and tumorigenesis.
Considering Type 2 DM as an inflammatory disease (like inflammatory bowel disease, connective tissue diseases, etc.), the present study aimed to assess the percentages of circulating Treg cells in patients with Type 2 DM, as compared to a group of healthy controls.
In the study, 50 Type 2 DM patients and 30 controls were recruited, and their blood samples were examined by flow cytometry for CD4+, CD25+ and FoxP3+ as markers for Treg cells. FBG, 2hPP and BMI were assessed for all participants. In addition, HbA1C and urinary protein/creatinine ratio were assessed for all patients. Other laboratory, radiological and interventional results were extracted from the files of patients who were attending the Endocrinology and Diabetes Outpatient Clinic of Ain-Shams University Hospital.
We demonstrated that:
• Percentages of Treg cells were lower among patients with Type 2 DM than among healthy controls.
• Percentages of Treg cells were lower among obese and overweight patients than among patients with normal BMI.
• Percentages of Treg cells were lower among patients with diabetic nephropathy than among those without.
• Percentages of Treg cells were lower among patients with uncontrolled diabetes than among those with controlled diabetes.
• Percentages of Treg cells were lower in older patients, and those with longer disease duration (and in turn were lower in those on insulin therapy).
• Percentages of Treg cells among patients did not differ according to gender.
• Percentages of Treg cells among patients did not differ according to the presence or absence of diabetic neuropathy.
• Percentages of Treg cells among patients did not differ according to the presence or absence of hypertension, dyslipidemia or IHD.
In conclusion, we confirm a possible role for Treg cells in Type 2 DM, as there was a significant reduction of Treg cell percentages among patients with Type 2 DM which correlated with BMI, disease duration, disease control and the occurrence of diabetic nephropathy.