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Protein Reverses Type 1 Diabetes

By Stephen Luntz

The protein CD52 suppresses immune responses and could stop autoimmune diseases like Type 1 diabetes, according to a report in Nature Immunology.

“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,” says Prof Len Harrison of the Walter and Eliza Hall Institute. “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.”

While Type 1 diabetes has been overtaken in frequency by Type 2 diabetes, rates have still doubled over the past 20 years. “It causes significant long-term complications involving the eyes, kidneys and blood vessel damage,” says Harrison. He says his team has “published studies showing that the increase is a result of people with lower risk genes being pulled in by environmental factors such as vitamin D deficiencies and lack of sleep. We’re not sure if CD52 is relevant to this.”

Irrespective of the causes, Harrison is very hopeful that CD52 could be used to not only stop the progression of diabetes but reverse it. He says a population of CD52-releasing T cells normally keeps the immune system in balance, and their removal leads to rapid development of diabetes in mice. “In animal models we can prevent and cure Type 1 diabetes using intravenous application of CD52,” Harrison says. “I am hopeful that these results will be translatable into humans, hopefully in the not-to-distant future.”

Prospects are naturally best at early stages, but Harrison says there have been “many attempts to preserve residual beta cell function” for patients with diabetes. Some attempts have been successful, indicating that it may be possible for CD52 to help the recovery of people who already have serious diabetes complications.

A non-specific immune suppressant could make the body more vulnerable to infections or cancers, but Harrison thinks that CD52 is specific enough that this may not be a problem. He says it is “not associated with any obvious reason to suspect side-effects, nor likely to generate an immune response against itself, which is a problem for other available treatments”.

Harrison’s team is using animal models to investigate whether CD52 also has applications for the fight against other common autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. They anticipate that clinical trials are several years off, even against diabetes, and suspect it would have to be taken by injection rather than orally.