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Immune Protein May Prevent the Progression of Type 1 Diabetes

Jun 6, 2013

Scientists determine an immune protein, CD52, suppresses the autoimmune response against pancreatic beta cells….

New research has identified an important role of a circulating immune protein on the surface of lymphocytes with implications for treating type 1 diabetes as well as other autoimmune diseases. Researchers from the Walter and Eliza Hall Institute’s Molecular Medicine division in Melbourne, Australia, identified the immune protein CD52 and its role in suppressing the body’s own immune response. Professor Len Harrison and his colleagues also studied the implications of CD52 as a potential treatment or prevention in the development of 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," Harrison reported. "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."

The autoimmune destruction of insulin producing beta cells leads to the development of type 1 diabetes most commonly in children and teenagers. Type 1 diabetes is among other debilitating autoimmune disease such as multiple sclerosis or rheumatoid arthritis that can develop long term complications if not manage properly. Utilizing the role of CD52 could greatly improve the management of controlling or suppressing the body’s errant immune response. Harrison and colleagues reported, "We identified a specialized 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."

To further understand the importance of CD52 expression, the research group studied the effects of depleted CD52 in mice. They reported, "In diabetes-prone mice of the nonobese diabetic (NOD) strain, transfer of lymphocyte populations depleted of CD52hi cells resulted in a substantially accelerated onset of diabetes."

Harrison further clarified their results, "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 autoimmune disease, and that CD52 has great potential as a therapeutic agent."

Harrison and colleagues looked at the correlation between CD52 depletion and type 1 diabetes. They reported "The proportion of CD52hiCD4+ T cells was significantly lower in the groups with preclinical and established type 1 diabetes than in the healthy group or the group with type 2 diabetes."

Professor Harrison concluded, "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."

Esther Bandala-Sanchez, Yuxia Zhang, Simone Reinwald, James A Dromey, Bo-Han Lee, Junyan Qian, Ralph M Böhmer, Leonard C Harrison. T- cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10. Nature Immunology, 2013; DOI