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  GM stem cells treat autoimmune disease
Mice with a human equivalent of multiple sclerosis have been successfully treated using genetically modified stem cells, say a group of Australian researchers.

The work, led by Dr James Chan of Monash University's Centre of Inflammatory Diseases, may lead to the development of a similar technique to treat autoimmune diseases in humans.

Autoimmune diseases, such as type 1 diabetes and multiple sclerosis, are caused when immune cells, called T cells, incorrectly identify proteins created by the body as foreign objects, such as bacteria, and attack them.

To prevent theese rogue T cells from entering the bloodstream, the immune system lures them with 'self-proteins' while they are developing in the thymus. T cells that bind tightly to these self-proteins are destroyed by the body's immune system.

Some slip through this 'net' and for some people result in auto-immune disease.
Fully recovered

Chan and colleagues genetically modified a specific type of stem cell, which produce more self-protein to ensure that dangerous T cells are more effectively removed from the system.

In the study, which appeared in the Journal of Immunology, mice were inoculated to develop experimental autoimmune encephalomyelitis (EAE), the human equivalent of multiple sclerosis. The genetically modified stem cells were then transplanted into the mice.

"After the transplantation, the mice are completely resistant to disease," says Chan.

While initial results are promising, Chan says human clinical trials would not be possible for some time.

"Before we transplant the stem cells we wipe out the immune system of the mice using high doses irradiation," says Chan.

He says this level of irradiation would not suitable for humans.

The team is now looking at ways of overcoming the need for radiation, in order to make the procedure clinically viable.
Promising

Dr Carola Vinuesa of the John Curtin School of Medical Research at the Australian National University in Canberra, says the results are "very exciting and potentially very promising."

But Vinuesa cautions that it is unclear how well the mouse model relates to human disease.

"The EAE mouse model of multiple sclerosis is not a model in which autoimmune disease develops spontaneously, as occurs with multiple sclerosis in humans," she says.

She adds there is still a lot we don't know about how healthy T cells know not to attack self-proteins.

"The mechanism by which they do this is still unclear, but the results [from this study] are spectacular," says Vinuesa.
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