Immune Protein Could
Stop Diabetes in Its Tracks, Discovery Suggests
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'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. 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."
This
research was supported by the National Health and Medical Research Council of
Australia and the Victorian Government.
Story Source:
The
above story is reprinted from materials provided byWalter and Eliza Hall
Institute.
Note: Materials may be edited for content and length. For further
information, please contact the source cited above.
Journal Reference:
1.
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:10.1038/ni.2610
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Walter and Eliza Hall Institute (2013, May 20). Immune protein could
stop diabetes in its tracks, discovery suggests. ScienceDaily.
Retrieved May 20, 2013, from http://www.sciencedaily.com/releases/2013/05/130520104932.htm
