Germs
could play a role in the development of type 1 diabetes by triggering the
body's immune system to destroy the cells that produce insulin, new research
suggests.
Scientists have previously shown that killer T-cells, a type of white blood cell that normally protects us from germs, play a major part in type 1 diabetes by destroying insulin producing cells, known as beta cells.
,
Scientists have previously shown that killer T-cells, a type of white blood cell that normally protects us from germs, play a major part in type 1 diabetes by destroying insulin producing cells, known as beta cells.
,
now using Diamond Light Source, the UK's synchrotron science facility to shine
intense super powerful X-rays into samples, a team from Cardiff University's
Systems Immunity Research Institute found the same killer T-cells that cause
type 1 diabetes are strongly activated by some bacteria.
The team hope this research will lead to new ways to diagnose, prevent or even
halt type 1 diabetes.
Cardiff University's Professor Andy Sewell, lead author of the study, said:
"Killer T-cells are extremely effective at killing off germs, but when
they mistakenly attack our own tissues, the effects can be devastating."
"During type 1 diabetes, killer T-cells are thought to attack pancreatic
beta cells. These cells make the insulin that is essential for control of blood
sugar levels.
"When beta cells are destroyed, patients have to inject insulin every day
to remain healthy."
Unlike type 2 diabetes, type 1 diabetes is prevalent in children and young
adults, and is not connected with diet. There is little understanding of what
triggers type 1 diabetes and currently no cure with patients requiring
life-long treatment.
In previous studies the Cardiff team isolated a killer T-cell from a patient
with type 1 diabetes to view the unique interaction which kills the
insulin-producing beta cells in the pancreas.
They found these killer T-cells were highly 'cross-reactive', meaning that they
can react to lots of different triggers raising the possibility that a pathogen
might stimulate the T-cells that initiate type 1 diabetes.Cardiff University's Dr David Cole said: "Killer T-cells sense their
environment using cell surface receptors that act like highly sensitive
fingertips, scanning for germs.
"However, sometimes these sensors recognise the wrong target, and the
killer T-cells attack our own tissue. We, and others, have shown this is what
happens during type 1 diabetes when killer T-cells target and destroy beta
cells.
"In this new study, we wanted to find out what was causing these T-cells
to kill beta cells. We identified part of a bug that turns on killer T-cells so
they latch onto beta cells. This finding sheds new light on how these killer
T-cells are turned into rogues, leading to the development of type 1
diabetes."
The research, published in The Journal of Clinical Investigation, provides a
first ever glimpse of how germs might trigger killer T-cells to cause type 1
diabetes, but also points towards a more general mechanism for the cause of
other autoimmune diseases.
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