New hope for rheumatoid arthritis sufferers as Melbourne researchers make new discovery

Aussies living with rheumatoid arthritis now have new reason to hope after Melbourne researchers uncovered a key immune driver behind the disorder.

Melbourne researchers have uncovered for the first time a key immune driver of rheumatoid arthritis, a painful and incurable condition affecting almost half a million Australians.

The finding paves the way for the development of new ways to treat and diagnose the chronic auto-immune condition, and block the way the body attacks its own joints.

There are particular immune proteins, that put people at higher risk of developing rheumatoid arthritis.

Co-lead author Hugh Reid, from the Biomedicine Discovery Institute at Monash University, said by understanding at the molecular level how the immune cells are able to connect and bind with the body’s joints in a misguided attack, was key to devising new ways of stopping this interaction.

Working with researchers from the US and Sweden for the past seven years, they looked at this immune interaction in mice and in human tissue. They also analysed this cellular interaction in a never-before-seen-way for this disease at the Australian Synchrotron.

Rheumatoid arthritis is a painful and incurable condition affecting almost half a million Australians.

Through this, they found that in those at higher risk had altered immune proteins in the joints which were “sticky”, allowing them to more easily bind to immune cells.

Consequently, this interaction meant they were mistakenly recognised as a foreign body and so kickstarted the inflammatory response that is the hallmark of the disease.

Capturing the molecular snapshot of this disease “trigger” is a first, said Dr Reid.

“It’s the first time we’ve been able to see and understand the role played by these high-risk immune genes and their association with rheumatoid arthritis development, at the molecular level,” Dr Reid said.

“We’re seeing the trigger. It’s a launching point for looking at better therapeutics to reduce the symptoms; the joint pain and swelling that people experience. The idea is we could use this information to short-circuit that interaction.

“This is a building block in the wall towards a cure, or try to alleviate the disease by providing better drugs.”

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