The mechanism of β cell destruction in Type 1 diabetes is not exactly known, Our hyphotesis is that interferon gamma, interleukin-2 and tumor necrotizan factor alpha have impotant roles in β cell destruction.

T helper (h)1 cells are known to have important roles in the destruction or/and dedifferentiation of β-cells in type 1 diabetes (T1D). Significant increase in IFN-γ-producing Th1 cells in the pancreas and in the serum levels were determined in type 1 diabetic patients at diabetes oneset. This data indicated that this proinflammatory mediator serve as a biomarker of advanced autoimmunity. We aimed to investigate the relationship between Th1 cytokines (IFN-γ, IL-2 and TNF-α) and T1D and the effect of those cytokines on β-cell function.

Inclusion Criteria:

• Patients giving consent to participate the study
• Patients with type 1 diabetes according to WHO definiton

Exclusion Criteria:

• Acute and chronic inflammatory diseases,
• significant concomitant diseases which may interfere with glucose metabolism
• cancers,
• hemoglobinopathies,
• recently received antibiotics,
• drugs influencing β-cell function and
• insulin sensitivity or anti-inflammatory drugs
• recent history of trauma

The study included 98 T1DPs and 30 healthy subjects (CG). All subjects

were matched on age and gender. β-cell function of 98 T1DPS was assesseed by measuring C-Peptide levels

after mixed-meal tolarence test (MMTT)s. T1DPs were divided into 3

groups according to the C-Peptide levels after MMTTs and the groups

were as follows: patients with undetectable ≤0.1 ng/mL(group 1a, n=30)

C-Peptide levels; minimal 0.1-0.8 ng/mL(group1b, n=30); and sustained

≥0.8ng/mL(group1c, n=38) C-peptide levels which increased at the 90th

minute after the meal ≥150% of fasting C-peptide level.