Protein for progressing autoimmune diseases identified

University of Adelaide researchers have identified the key protein involved in driving the progression of multiple sclerosis (MS) and other autoimmune diseases through the body’s ‘super-inflammatory’ immune response.

The confirmation of the protein brings scientists one step closer to blocking the development of MS — an incurable neurodegenerative disease — as well as other autoimmune diseases which affect more than 2.5 million people worldwide.

The protein in question is a chemokine receptor involved in moving the body’s immune response cells (T-cells) around the body when they are in the super-inflammatory mode needed to fight persistent infections — or, in the case of autoimmune diseases like MS, attacking the body’s own tissues. The receptor CCR6 was widely assumed to be involved in this process, but according to project leader Professor Shaun McColl, this was incorrect.

“Everybody has been focusing on the CCR6 receptor as the one to target to control this inflammatory response,” said Professor McColl, director of the Centre for Molecular Pathology at the University of Adelaide.

“We’ve now shown that the receptor to target is actually CCR2.”

The discovery was made when the researchers tested the immune response that occurs in MS on three groups of genetically modified mice. Professor McColl explained, “We used one strain of mice that didn’t exhibit CCR6 and another that didn’t exhibit CCR2, and a control or ‘normal group’ to use as a comparison.”

Writing in the journal Nature Communications, Professor McColl and his team revealed that blocking CCR6 actually made the MS worse. But when the researchers tested the mouse without CCR2, they found “complete inhibition of the disease”, Professor McColl said.

“If we can find an antagonist to block the CCR2 receptor specifically on these T-cells, we should be able to control the progression of MS,” he continued.

In addition to blocking receptors in order to halt disease development, the researchers also believe their study may lead to improved vaccines to fight infection.

“Unlike in autoimmune diseases, where the body’s immune response is destroying its own cells and the aim is to block T-cell migration, with persistent infection we want to turn on the super-inflammatory response and enhance the migration of the immune cells to sites where they are needed,” said Professor McColl. “This research may help guide development of vaccines that can better force that immune response.”

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