Introduction: Type 1 diabetes mellitus (T1DM) is a complicated autoimmune disorder that is marked by the destruction of pancreatic islands by T cells. It is widely believed that genetic factors play a crucial role in the development of T1DM and other autoimmune diseases. At present, the contribution of the gene cytotoxic T-lymphocyte antigen-4 (CTLA4) to type 1 diabetes has not been fully determined. Objectives: The primary objective of this research was to examine the relationship between the CTLA-4 -1722T/C (rs733618) and -318 C/T (rs5742909) polymorphisms and the onset of T1DM in Iraqi children. Patients and Methods: In this case-control study, a total of one hundred children were examined. Specifically, fifty children diagnosed with T1DM and fifty age and sex-matched non-diabetic children were recruited as controls. The polymerase chain reaction (PCR) technique was employed using the allele-specific PCR method to analyze the CTLA-4 -1722T/C (rs733618) and -318 C/T (rs5742909) polymorphisms. The levels of glutamic acid decarboxylase antibody (anti-GAD Ab), anti-islet antigen-2 antibody (anti-IA-2 Ab), and insulin were determined using the enzyme-linked immunosorbent assay (ELISA) method. Results: Children with T1DM showed significantly higher levels of anti-IA2 and anti-GAD than healthy controls, while patients had significantly lower levels of insulin than healthy controls. However, there was no statistically significant relationship between CTLA-4 polymorphisms -1722T/C (rs733618) and -318 (rs5742909) and anti-GAD Ab, anti-IA-2 Ab, with insulin levels in T1DM patients and controls. Conclusion: The findings of the present investigation indicate that neither CTLA-4 polymorphism -1722T/C (rs733618) nor CTLA-4 polymorphism -318 (rs5742909) are associated with genetic predisposition to T1DM.
khudair et al. (Thu,) studied this question.