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| Professor Richard Kitching |
Monash University researchers have discovered the mechanism that
explains how key genetic risk factors cause or protect people from autoimmune disease such as kidney disease, type 1 diabetes, multiple sclerosis, and Crohn’s disease.
Published last week in Nature, Monash researchers have
answered the fundamental question: why, and how, does having different immune molecules change a person’s
underlying genetic risk of developing an autoimmune disease?
Autoimmune diseases affect over 1 million Australians and, in
the Western world, are a leading cause of death in women under the age of 65. These diseases include type
1 diabetes, multiple sclerosis, Crohn’s disease, ulcerative colitis, rheumatoid arthritis and several types
of kidney disease.
Monash University co-senior author, Professor Richard Kitching,
explained that our immune system has evolved to fight infections and disease.
“Our immune system is able to protect us from foreign invaders,
as it learns to recognise different infections over time,” Professor Kitching said.
“But, this sometimes goes wrong and our immune system recognises
parts of our own body as being foreign. This leads to autoimmune disease.”
Professor Jamie Rossjohn, co-senior author, ARC Laureate Fellow
and Chief Investigator on the ARC Centre of Excellence in Advanced Molecular Imaging, said that
autoimmune diseases occur when our immune system produces an aberrant response against our own
cells, tissues and/or organs, resulting in
inflammation and damage.
“Certain immune molecules, called HLA molecules, are associated
with an increased genetic risk to cause autoimmunity, whereas other HLA molecules can protect from
disease,” Professor Rossjohn said.
Professor Kitching said their research provided the first
mechanistic evidence of the basis of protective and disease causing HLA molecules in autoimmunity.
“Our research has given us a new understanding of why some
people are at risk of disease, while others are protected,” Professor Kitching said.
“We have known that in autoimmune diseases there are T cells
that make us susceptible to disease and T cells that protect us from disease. Now we know how this
happens; it opens the field for new and more targeted treatments to specific diseases.
“In Goodpasture’s disease when the molecule DR15 is present it
can select and instruct T cells to attack the body. If alone in our body these damaging cells can attack
the body’s tissues, resulting in very ill patients.
“But when people also have the protective DR1 molecule present
these T cells are held at bay and can be overturned,” Professor Kitching said.
This research is the first mechanistic evidence of what causes
our immune system to go rogue and attack parts of our own body. It paves the way for further
research and for new and novel treatments, as well as avenues that lead to personalised therapies.
“We have answered one of the biggest questions in autoimmune
disease,” Professor Rossjohn said.
“There is evidence out there that this mechanism is relevant to
other autoimmune diseases and it opens up new lines of research into how autoimmune disease occurs.”
“These particular protective immune cells are specific and are
extremely powerful,” Kitching continued.
“So, if we can encourage them to develop in the body, or expand
people’s cells outside the body and inject them back into those with disease, this could result in better
and more targeted treatments for autoimmune
diseases,” he said.
Watch a video explaining the video HERE.
Watch a video explaining the video HERE.
