Immune protein could stop diabetes in its tracks
Melbourne researchers 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
the Walter and Eliza Hall Institute that identified the immune protein CD52 as responsible for
suppressing the immune response, and its potential for protecting against autoimmune diseases. The
research was published today in the journal Nature Immunology.
So-called autoimmune diseases develop when the immune system goes awry and attacks the body’s
own tissues. Professor 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,” Professor
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.”
Type 1 diabetes is an autoimmune disease that develops when immune cells attack and destroy
insulin-producing beta cells in the pancreas. Approximately 120,000 Australians have type 1 diabetes
and incidence has doubled in the last 20 years. “Type 1 diabetes is a life-long disease,” Professor
Harrison said. “It typically develops in children and teenagers, and it really makes life incredibly
difficult for them and their families. It also causes significant long-term complications involving the
eyes, kidneys and blood vessel damage, and at great cost to the community.”
Professor 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. 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 said.
CD52 appears to play a dominant role in controlling or suppressing immune activity in the early
stages of the immune response, Professor 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,” Professor Harrison said. “The cells act as
an early ‘braking’ mechanism.”
Professor Harrison said his goal is to prevent and ultimately cure type 1 diabetes. “In animal models
we can prevent and cure type 1 diabetes,” Professor Harrison said. “I am hopeful that these results
will be translatable into humans, hopefully in the not-too-distant future.”
The research was supported by the National Health and Medical Research Council of Australia and
the Victorian Government.
For more information contact Liz Williams, Media and Publications Manager, on +61 3 9345 2928, +61
405 279 095 or williams@wehi.edu.au.
Source: http://www.wehi.edu.au/uploads/MR2013_05_20_Harrison_CD52.pdf
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