ABSTRACT
Type 1 diabetes is an immune disease. The hallmark of the disease is initiation of inflammation of the beta-cells of the pancreas. T lymphocytes play an obligatory role in the islet cell inflammation. Both CD4+ and CD8+ T cells are needed to initiate the destruction of beta cells in many models. CD4+ T cells are subclassified into Th 1 cells and Th 2 cells. A number of studies implicated Th 1 cells in the development of type 1 diabetes. To evaluate the function of Th1 subset of T lymphocytes in recently diagnosed type 1 diabetic patients and high risk first degree relatives and compare it with normal subjects not at high risk of development of the disease. The study included 18 patients with recent onset type 1 diabetes [6 males and 12 females], 32 first degree relatives of patients with type 1 diabetes. The relatives were all chosen after being screened for islet cells antibodies; only those who were positive for islet cell antibodies were included. They were 10 males and 22 females,. A control group of 20 apparently healthy subjects [5 males and 15 females], their age ranged from 9-29 years [13.8+9.1]. For each studied subject blood was obtained -after overnight fasting- under strict aseptic conditions into three vacutainer tubes [Becton USA]:1. Heparin containing tube for cell culture. 2. EDTA containing tube for measurement of HbA[1c]. 3. Tube without additives. Blood in this tube was allowed to clot at room temperature and centrifugation was done at 1000 xg. Serum was separated and stored at -70°C until the essay for IL-12, IFN-y, C peptide and islet cell antibodies. The levels of both IL-12 [a potent inducer of Th 1 cells], and INF-y [a potent product of Th 1 cells] are higher in the serum of both type 1 diabetic patients and high risk relatives. IFN-y and /L-12 was higher in culture supemates of the whole blood of both diabetics and high risk relatives [in vitro]. There was no significant difference between the diabetic patients and high risk relatives in the level of either IL-12 or IFN-y either in vivo or in cell culture production. In the evolution of type 1 diabetes; there is increased production of IL-12 leading to shift towards Th 1 rather than Th 2 response allowing increased production of Th 1 cytokines including IFN-y. This may initiate a cascade of immune/ inflammatory process culminating in beta cell destruction