Using one type of immune system cell to turn off another stopped type-1 diabetes in mice, U.S. researchers said on Monday.

The study suggests it may be possible to retrain a faulty immune system, stopping it from attacking the pancreas and causing type-1 or juvenile diabetes, the researchers said.

Writing in the Journal of Experimental Medicine, Kristin Tarbell and colleagues at Rockefeller University in New York said they used immune system cells called dendritic cells to stimulate production of suppressor T-cells.

These T-cells turn off the body’s faulty immune response. In the case of the mice, they stopped the destruction of their pancreatic islet cells that causes type-1 diabetes.

Type-1 or juvenile diabetes is an autoimmune disease, caused when immune cells for unknown reasons destroy healthy tissue. In diabetes, they kill off the cells in the pancreas that make insulin.

An estimated 2 million Americans have type-1 diabetes.

“You have to stop the immune system from attacking those pancreatic islet cells,” Tarbell said in a statement

“Instead of silencing the attackers directly, we learned how to generate another type of cell, called a regulatory or suppressor cell, which essentially turns off the attackers,” Tarbell added.

What works in mice may not necessarily work in people, the researchers caution.

But the immune systems are highly similar.

Dendritic cells signal to T-cells, helping them identify which invaders to attack and which to tolerate.

For their study, the Rockefeller team removed suppressor T-cells from the mice, grew more of them in lab dishes, and injected them back into the mice. They also purified the compounds used by dendritic cells to signal the T-cells and used them to make the suppressor-T-cells proliferate.

For the method to work, diabetes will have to be diagnosed very early, Tarbell noted.

“If this method for restoring the balance of suppressor T-cells proves effective all the way through our research and into humans, we still need to intervene before the islet cells are completely destroyed,” Tarbell said.

“Measuring early onset will be just as important as treating it.”