Role of the HIP2.5 Specific CD4+ T Cells in Islet Inflammation
Type 1 diabetes is an autoimmune disease where the immune system develops reactivity toward beta cells, the insulin-producing cells of the pancreas. The disease is primarily caused by the T cells of our body developing specificity/reactivity to certain self-antigens secreted by the beta cells. A variety of autoreactive T cell populations have been identified. Here we investigate the role of one of these populations, the HIP2.5 specific CD4+ T cells, in disease progression. To understand the role of HIP2.5, mice were treated with an antibody (1A1) that blocks the HIP2.5 peptide from being 'seen' by CD4+ T cells. Histological analysis of the pancreata of these mice showed that the 1A1 antibody treatment led to significantly decreased levels of CD4+ T cells infiltrating and surrounding the beta cell clusters in the pancreas. These mice also had greater levels of insulin remaining within the beta cell clusters. The decrease in bulk CD4+ T cells seen with 1A1 treatment indicates that the HIP2.5 specific CD4+ T cell population can impact other populations of T cells. In the future, this type of treatment could be paired with an early detection test for diabetes to proactively stop beta cell destruction in humans, essentially delaying or entirely preventing diabetes.