Scientists have identified an immune protein that has the potential to stop or reverse the development of Type-1 diabetes in its early stages, before insulin-producing cells have been destroyed.
The discovery has wider repercussions, as the protein is responsible for protecting the body against excessive immune responses, and could be used to treat, or even prevent, other immune disorders such as multiple sclerosis and rheumatoid arthritis.
Professor Len Harrison, Dr. Esther Bandala-Sanchez and Dr. Yuxia Zhang led the research team from Australia’s Walter and Eliza Hall Institute’s Molecular Medicine division that identified the immune protein CD52 as responsible for suppressing the immune response, and its potential for protecting against autoimmune diseases.
Autoimmune diseases develop when the immune system goes awry and attacks the body’s own tissues. Mr. Harrison said CD52 held great promise as a therapeutic agent for preventing and treating autoimmune diseases such as Type-1 diabetes.
“Immune suppression by CD52 is a previously undiscovered mechanism that the body uses to regulate itself, and protect itself against excessive or damaging immune responses,” Mr. Harrison said.
“We are excited about the prospect of developing this discovery to clinical trials as soon as possible, to see if CD52 can be used to prevent and treat Type-1 diabetes and other autoimmune diseases. This has already elicited interest from pharmaceutical companies,” Mr. Harrison said.
Type-1 diabetes is an autoimmune disease that develops when immune cells attack and destroy insulin-producing beta cells in the pancreas.
Harrison said that T cells that have or release high levels of CD52 are necessary to maintain normal balance in the immune system.
“In a preclinical model of Type-1 diabetes, we showed that removal of CD52-producing immune cells led to rapid development of diabetes,” he said.
“We think that cells that release CD52 are essential to prevent the development of autoiummune disease, and that CD52 has great potential as a therapeutic agent,” he added.
CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Mr. Harrison said.
“We identified a specialised population of immune cells (T cells) that carry high levels of CD52, which they release to dampen the activity of other T cells and prevent uncontrolled immune responses. The cells act as an early ‘braking’ mechanism,” Mr. Harrison said.
“In animal models we can prevent and cure Type-1 diabetes. I am hopeful that these results will be translatable into humans, hopefully in the not-too-distant future,” Mr. Harrison said.
The study was published in the journal Nature Immunology.