Recent Onset type 1 diabetes
Type-1 diabetes (T1D) is a chronic illness characterized by the pancreas inability to produce insulin, and the subsequent loss of glycemic control leading to deleterious clinical symptoms (asthenia, polyuria, weight loss, increased risk of infection, etc.). T1D arises from progressive autoimmune destruction of the beta pancreatic islets.
Pathophysiology
The development of T1D results from the interplay of environmental exposures and numerous genetic susceptibility variants across the genomes. Indeed, in addition to the HLA class I and II genes providing the pivotal susceptibility for the T1D, other genes related to the IL-2 pathway, Treg cell activation and immune tolerance are involved (Todd et al. 2010). The PTPN22 (protein tyrosine phosphatase N22) may induce B and T-cells activation in an uncontrolled manner increasing the overall immune system reactivity. The IL-2RA gene encoding the α chain of the high-affinity IL-2 receptor (CD25) is associated with an immune imbalance between regulatory T cells and effector T cells.
Furthermore, a deficit of IL-2 and/or Treg cell deregulation are widely recognized as a key driver of T1D pathophysiology.
Epidemiology
T1D onset most often occurs in childhood with more than 98,000 children under 15 years developing the disease worldwide annually but the disease can also develop in adults. Over the last decades, this incidence is estimated to increase by 3 % each year worldwide. Yearly, about 100,000 patients are newly diagnosed with T1D in the USA and Europe. In prevalence, T1D affects about 20 million people worldwide representing 10% of type 1 and type 2 diabetes prevalence.
Disease management
Exogenous insulin constitutes for many years the sole treatment for T1D although it does not cure the disease. Insulin therapy allows to achieving short-term metabolic control but in about 50% of patients this control is largely imperfect. It triggers in return deleterious mid- to long-term complications such as retinopathy, heart diseases and stroke, nerve damage, etc.
What does ILTOO Pharma bring?
ILT-101 is intended to be administered as soon as T1D is diagnosed. It is expected to block the autoimmune process by stopping the β-pancreatic islets destruction and therefore sustaining natural insulin secretion and metabolic control in patients benefiting from a residual pancreatic beta cell function. This can ultimately lead to a reduction in the complications (retinopathy, nephropathy, atherosclerosis…) associated with repeated and long-term use of exogenous insulin.