Genetic variation, biological structure, sources, and fundamental parts played by CXCL12 in pathophysiology of type 1 diabetes mellitus

Type I diabetes (TID) is defined as an autoimmune disease resulting from the destruction of insulin-producing beta-cells by autoreactive T cells. It is believed that TID resulted from the immune-mediated destruction of insulin-producing β-cells in pancreatic islets of Langerhans. Chemokines are small glycoproteins (weighing 8–10 kDa) that are attractive chemotactive factors for a wide variety of cell types, especially immune system cells and their target cells which express appropriate G protein receptors. It has been well established that chemokines as the main arms of the immune system play key roles in the regulation of immune responses which is evidenced to be important in the pathogenesis of the diseases. Several other environmental and genetic components of the immune systems also confirmed to influence the onset of immune-related diseases. The CXC chemokine CXCL12 is involved in the development of immune responses. Previous studies reported that the known genetic variation SDF1–3′A regulates the expression of CXCL12. Hence, the aim of this study was to address the latest findings regarding the relation between the serum concentrations and CXCL12 genetic variation, in SDF1–3′A in T1D.