Techniques to genetically modify patient immune cells have revolutionized the fight against hard-to-treat cancers. But they can come with dangerous side effects. Now, researchers have found one reason why. WorldCancerDay
Dying cells had high levels of a cellular protein called gasdermin E, or GSDME, which punctures the cell membrane, the team found. Nearby immune cells picked up on distress signals from the exploded cell and released cytokines that set off inflammation, Huang says.
When GSDME was blocked, the cancer cells succumbed in a less messy way: They probably wilted instead of exploding, causing less damage, the team found. Mice injected with CAR-T cells and cancer cells lacking this protein still had symptoms of cytokine release syndrome, Huang says, but the symptoms were mild and fewer mice died.
The results hint at a starting point to find a way to reduce severe side effects of CAR-T cell therapy, although treatments for people are probably far off. One approach might be to block GSDME to ensure cancer cells die without producing distress signals, Huang says. Another is to find ways to prevent other parts of the immune system from responding when edited T cells attack cancer cells, but that could leave patients vulnerable to infection.
“It’s a great step forward,” says Theodore Giavridis, an immunologist and cellular engineer at ArsenalBio, a precision immunotherapy company in San Francisco, who was not involved in the work. If the findings hold up, they would boost understanding of cytokine release syndrome. But it’s possible that blocking pyroptosis from happening at all will make CAR-T cells less effective, Giavridis says.
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