In results published by a researcher at the University of Adelaide, it is suggested that it's possible there is a new mechanism to control multiple sclerosis (MS).
A three year fellowship from MS Research Australia has been awarded to Dr. Iain Comerford from the University's School of Molecular and Biomedical Science to work on a project. The project is to determin if specific enzymes in immune system cells have an effect on regulating immune cell activation and migration.
With his colleagues in the project, Professor Shaun McColl and PhD students Wendel Litchfield and Ervin Kara, they focused on a molecule involved in the activation and movement of white blood cells. This molecule is known as PI3Kgamma.
"There's already been worldwide interest in PI3Kgamma in relation to other human inflammatory disorders, such as diabetes and rheumatoid arthritis, and our study links this molecule and MS," said Dr Comerford, who is a Multiple Sclerosis Research Australia Fellow at the University of Adelaide.
In an animal model developed as a standard laboratory system for studying MS, Dr. Comerford and his colleagues have shown this molecule crucial for the development of an experimental autoimmune encephalitis (EAE).
The team has shown that a genetic alteration can knock out that particular molecule. Resulting in a high resistance to the development of EAE. Thereby protecting the nervous system from damage typical of MS.
Severe damage to the myelin in the central nervous system was evident with the presence of this molecule. This resulted in inflammation in the spinal cord and myelin loss.
After these results the team used an orally active drug blocking the activity of molecule PI3Kgamma at the first signs of disease onset. The drug suppressed the development of EAE also reversing clinical signs of the disease.
"Our results so far have been very promising," Dr Comerford said.
"We've shown that by blocking PI3Kgamma, we can reduce the activation of self-reactive immune cells, reduce the release of inflammation-inducing molecules from immune cells, and also result in a dramatic reduction in the movement of immune cells into the central nervous system.
"Our hope is that future therapies for MS might target this molecule, which could very specifically dampen the damaging inflammation in the central nervous system
"It will now be crucial to determine whether targeting these molecules could be a safe and effective way to treat MS in humans," Dr Comerford said.
Mr Jeremy Wright, CEO of MS Research Australia, said: "It is very rewarding to see that MSRA has been able to support these exciting developments by a young up-and-coming researcher. We will await his further results with great interest."
William D.
