Unidentified Polymorphism in Ip-10/CXCL10 Gene linked to Type 1 Diabetes

The development of insulin dependent type 1 diabetes (T1D) is considered to be an autoimmune proinflammatory process mediated by T-cell destruction of pancreatic beta cells. It is believed to be triggered by some environmental factors and human enteroviruses are among the candidates. After infection the virus enters beta cells and triggers the expression of immunological factors as chemokines, interferons, interleukins which attract and activate autoreactive immune cells. The attracted and activated immune cells destroy infected beta cells. The viruses may trigger T1D, but the genes play important role in this process. Improved knowledge of gene polymorphisms of chemokines and their receptors could be useful to predict the onset of diabetes and define its progression. When searching for polymorphisms in the genes encoding chemokines MIG/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11 I found a difference in the IP-10 gene between patients with type 1 diabetes and control patients. Identification of this polymorphism would give more light and explanation for the reason and mechanism by which some individuals develop autoimmune diabetes. This knowledge would help us develop a strategy for prediction and prevention of T1D. These investigations will contribute to fighting diabetes on national and international level. The chemokine IP-10 expressed from pancreatic beta cells and its receptor CXCR3, expressed on the surface of immune cells are of interest as a predictive marker for the risk assessment of the autoimmune destruction of beta cells. By screening the people for this polymorphism we may be able to identify the predisposed to T1D individuals in early childhood and prevent the development of T1D by trying different experimental preventive therapies and approaches.