
Stanford University researchers have discovered a previously unknown type of immune cell in planarian flatworms that destroys nearby cells by exploding. The team named these cells ruptoblasts, and the process they trigger — a rapid, localized self-destruction — ruptosis. When a specific hormone called activin spikes (for example, due to tissue fusion, injury, or bacterial infection), ruptoblasts undergo a sharp calcium surge from their endoplasmic reticulum, causing them to burst open within seconds to minutes. They release toxic substances that kill neighboring cells — such as E. coli bacteria, human kidney cells, or mouse blood cells — before the ruptoblast itself vanishes completely, leaving virtually no trace. What makes this particularly unusual is the speed: while some other organisms can undergo explosive cell death, it typically unfolds over several hours as contents slowly leak out. Ruptosis is much faster. The discovery began when postdoctoral researcher Chew Chai was testing whether flatworms could distinguish their own tissue from that of another worm; she observed this dramatic inflammatory response during tissue rejection. The study, published in Cell, suggests this ancient immune strategy may have evolved long before more familiar defenses like white blood cells. The researchers believe this mechanism could inspire new approaches to targeting infections or tumors in the future.