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A protein that could be harnessed to prevent or reverse the onset of type 1 diabetes has been identified by Australian researchers.<br />
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The researchers found the protein - CD52 - plays a key role in protecting the body against excessive immune responses, and could be used to treat other autoimmune disorders such as multiple sclerosis and rheumatoid arthritis.<br />
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Study leader, Professor Len Harrison, of the Walter and Eliza Hall Institute, says the team has already found CD52 prevents type 1 diabetes in mouse models and is confident of moving "quickly to clinical trials".<br />
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The findings, published today in Nature Immunology, focuses on the role CD52 plays in suppressing the body's immune response to the specific antigens that drive autoimmune disease.<br />
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Autoimmune diseases, such as type 1 diabetes, develop when the immune system begins to attack the body's own tissues.<br />
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The protein CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Harrison says.<br />
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Harrison and colleagues' findings follow on from their earlier discovery T cells, specialised immune cells, that regulate the activity of other T cells.<br />
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Harrison says this latest paper outlines the mechanism by which these regulatory T cells work.<br />
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Works like a brake<br />
The researchers found T cells that carry high levels of CD52 release the CD52 to "dampen down or put a brake on" the growth of T cells being activated by the disease-causing antigens.<br />
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Harrison says their work shows people with type 1 diabetes are less able to generate CD52 cells and therefore lose this protection.<br />
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They were able to demonstrate the link with the onset of the autoimmune disease as the removal of the CD52-producing immune cells in mouse models led to the rapid development of diabetes.<br />
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"The data we have so far indicates CD52 is an effective immune-suppressing agent so we are excited about its therapeutic potential," says Harrison.<br />
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The discovery of the protective mechanism could also provide a tool to identify people at risk of developing autoimmune diseases.<br />
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Harrison says he and colleagues have been able to measure a deficiency of this mechanism in laboratory tests and hope to ultimately screen for CD52 deficiency to pinpoint people at risk of specific autoimmune diseases.<br />
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He says boosting the levels of CD52 in people at risk may be one approach to developing a treatment for diabetes.<br />
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