Stanford researchers identified a new cell type in planarian flatworms that bursts within seconds to kill neighboring cells, then disappears. The discovery reshapes how scientists think about the evolution of immune defense.
In a flatworm, scientists have found an immune cell that kills its neighbors by exploding, then vanishes within minutes, leaving no trace.
The cell, which the Stanford team calls a ruptoblast, was uncovered in planarian flatworms, the freshwater animals famous for regenerating lost body parts. When a worm's own tissue meets tissue from a different individual, these cells trigger a violent self-destruct sequence that destroys everything within reach and then disappears, all in under five minutes. The researchers describe the behavior in a paper published this month in Cell, led by postdoctoral researcher Chew Chai in the lab of Bo Wang, an associate professor of bioengineering in the Stanford schools of Engineering and Medicine.
"This is a new effector cell, a new mechanism, in an organism that we already use to study regeneration and development," said Wang, in remarks reported by SciTechDaily. The team named the killing process "ruptosis" and the cells that perform it "ruptoblasts," a nod to the way they rupture as they kill.
The mechanism runs on a familiar molecular signal turned up to lethal volume. Activin, a hormone already known to help planarians regulate body size, triggers the ruptoblasts to release calcium from their endoplasmic reticulum. The cells swell, burst, and dump toxic contents into their immediate surroundings. Anything caught in that radius dies: in lab tests, the ruptoblasts killed E. coli bacteria, cultured human kidney cells, and mouse blood cells placed next to them. The destruction does not spread, and it does not linger. The ruptoblast itself is gone within about five minutes, the authors report, leaving a small, clean wound.
The discovery began with a curiosity experiment. The Wang lab grafted tissue from one planarian onto another, a kind of "Frankenstein worm" chimera. The recipient flatworm rejected the foreign tissue, but the response looked nothing like the T-cell-driven transplant rejection familiar from human medicine. Instead, the foreign tissue was chewed apart by an inflammation-like process the team had not seen before. The cells responsible turned out to be a previously unknown, non-blood lineage: glandular, anchored in the worm's body, and unrelated to the immune cells of vertebrates.
That non-mammal origin matters for how readers should weigh the result. Ruptoblasts are not white blood cells. They come from a different developmental lineage, and the Cell paper describes a strategy of immune defense that seems to have appeared early in animal evolution and then vanished. In a comparative search, the team found structures consistent with ruptoblasts only in basal bilaterians, the early-branching animals that include flatworms, and not in flies, nematodes, or vertebrates. The article does not enumerate the full species list, which independent immunologists are likely to check against the paper itself.
Wang's group offers a speculative but tidy explanation for why the strategy did not survive in larger animals. Planarians can regrow entire organs from a small fragment, they carry abundant pluripotent stem cells, and they tolerate wounds that would be fatal elsewhere. Ruptosis, with its localized but messy collateral damage, is a tolerable defense in an animal built to rebuild itself. In a vertebrate, the same blast radius would be catastrophic because most tissues cannot be replaced. Evolution, the authors suggest, traded ruptosis for a more contained immune response that does not destroy the body it is trying to save. "It opens up a new way of thinking about the evolution of immunity, not as increasing complexity but as different trade-offs," Wang told SciTechDaily.
The authors are careful to frame medical implications as a future question, not a near-term treatment. Ruptoblasts are fast, lethal on contact, and self-limiting. In principle, a controlled version of that chemistry could one day power a precision antimicrobial or anti-tumor strategy that kills diseased cells without spreading. That remains a hypothesis, and the Stanford announcement frames it as such. The practical gap between a flatworm's inflammatory burst and a human therapy is wide, and the discovery does not bridge it.
The team, which also includes Benyamin Rosental, Hawa Racine Thiam, and Christine Jacobs-Wagner, was supported by an NSF Graduate Research Fellowship, a Stanford Graduate Fellowship, a Stanford DARE fellowship, the Human Frontier Science Program, the NIH, and the European Research Council. The work appears in Cell, published 2 June 2026.
The next step is whether the ruptosis machinery exists in vertebrates at all, even in vestigial form, and whether any human cell type can be coaxed into a controlled version of the same burst. The Stanford lab says both questions are open.