Genetic molecule behavior responsible for human risk of autoimmune disease: Aussie study

Australian researchers have discovered how genetic factors can protect from or cause autoimmune diseases, a study published on Thursday revealed.

Published in the respected journal Nature, the study by researchers from Monash University has answered the age-old question of how different immune molecules can change a person's risk of developing autoimmune diseases.

The research is the first evidence ever found of what causes the immune system to "go rogue" and attack parts of the body.

Autoimmune diseases include type 1 diabetes, multiple sclerosis (MS), Crohn's disease, ulcerative colitis, rheumatoid arthritis and several types of kidney diseases and affect over 1 million Australians.

Richard Kitching, co-author of the study, said the human immune system has evolved over time to fight infections and disease.

"Our immune system is able to protect us from foreign invaders, as it learns to recognize different infections over time," Kitching said in a media release on Thursday.

"But this sometimes goes wrong and our immune system recognizes parts of our own body as being foreign. This leads to autoimmune disease."

Kitching said the different ways in which HLA molecules act from person to person was responsible for some people being at risk of autoimmune diseases while others were protected.

"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," he said.

"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," Kitching added.