Type I diabetes is a chronic autoimmune disease that occurs when the body's
immune system destroys insulin producing pancreatic beta cells.
Current treatments for type I diabetes focus on controlling blood sugar with
insulin therapy and must continue throughout a person's life.
The researchers focused on blocking the autoimmune process that destroys
beta cells and leads to diabetes, with the aim of developing therapies that can
prevent the illness from developing rather than treating its symptoms.
"None of the animals on the treatment developed diabetes even when we
started treatment after significant beta cell damage had already occurred. We
believe this type of treatment would slow the progression of type I diabetes in
people or potentially even eliminate the need for insulin therapy," said
Thomas Burris, chair of pharmacological and physiological science at Saint
In this study, researchers found that two nuclear receptors play critical
roles in the development of TH17 cells, and that by targeting these receptors,
they were able to stop autoimmunity from developing in several mouse models,
sparing beta cells.
They blocked the receptors with SR1001, significantly reducing diabetes in
mice that were treated with it.
These results confirmed that TH17 cells likely play a key role in the
development of type I diabetes and suggest that the use of drugs that target
this cell type may offer a new treatment for the illness.
The research was published in the journal Endocrinology.