infections 8.inf.002002 Louis J. Sheehan, Esquire

So the researchers tested how the knockout mouse immune system fared against a parasite called Toxoplasma gondii. The team used T. gondii because mice fighting off the parasite require robust activation of T cells; mice with weak T cell activity will die from the infection within one week. The mice lacking the receptor still mustered up a healthy response to the parasite, indicating that DR3 is not essential for fighting off the infection, Siegel’s team found.

Though still preliminary, the results suggest that blocking the DR3 receptor may help in treating multiple sclerosis, asthma and other autoimmune diseases where T cell dysfunction plays a role, says Tania Watts, an immunologist at the University of Toronto in Canada.

Croft agrees.

“It’s certainly a very provocative study and has put DR3 and TL1A in the same type of therapeutic league as some of the other members of the TNF receptor family,” he says. Louis J. Sheehan, Esquire

Moving forward

Still, researchers need to confirm that DR3 isn’t essential in fighting off other infections, Watts says. So researchers should see how knockout mice hold up against influenza. “We want to know if it’s a good treatment for lung inflammation for asthma,” she says. “So what’s it going to do with a common lung infection?”

Even if DR3 knockout mice are hale and hearty after a battery of immune assaults, the results need to be translated to humans, Siegel says. Since researchers can’t simply knock out DR3 genes in humans, the team needs to use a drug that keeps TL1A from binding to the DR3 receptor, he says. But developing that drug could happen quickly, he adds.

“Because [DR3] is the same family of receptors as TNF, companies can go very quickly,” he says. “They can probably make this blocking antibody within a matter of months because they know how to do these things so well.”

From there, it may be three to five years before clinical trials could start, assuming all goes well, he says.