‘Frankenstein’ proteins offer better control for immunotherapy

in BME Spotlight Faculty, BME Spotlight-Research, NEWS, Spotlight Faculty, Spotlight Research

by Barbara Moran | July 5th, 2018

Researchers have come up with a tool that offers a means of control over engineered cells, and it comes from a seemingly unlikely source: the hepatitis C genome.

In combination with a widely available antiviral medication, the new system offers a novel tool: a highly specific way to turn engineered cells on and off, with an existing, proven medication.

Most pharmaceutical drugs are blunt instruments against disease. Antidepressants send the whole brain swimming with serotonin. Antibiotics carpet-bomb all the bacteria in your gut, killing the good with the bad. Traditional chemotherapy attacks the fast-growing cells in your body, laying waste not only to tumors, but also hair follicles and bone marrow.

The field of synthetic biology—where scientists redesign existing biological systems to do new jobs—offers the promise of a more nuanced approach: cellular therapies that can work more precisely and selectively. What if, for instance, we could tweak the immune system to do our bidding—train it to attack tumors instead of saving its punch for foreign invaders?

This type of “immunotherapy” is a long-standing goal of modern biology, and for some cancers, like non-Hodgkin’s lymphoma, it’s already proving effective. But for immunotherapy—and for all medicines based on living human cells—there’s a sticky problem: once you train cells to attack a tumor, or kill bacteria, or build cartilage in an arthritic knee, how do you turn them off when the job is done?

“A challenge for doctors will be to control these living entities while they are in the body, allowing them to carry out their curative properties while not letting them get out of hand,” says John Ngo, assistant professor of biomedical engineering at Boston University. “This is a new paradigm, and the rules regarding how to control therapeutic cells still remain to be written.”

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