Schistosomes are a type of parasitic flatworm, or fluke, and inhabit a site in the human body that is inhospitable to most other parasites – the blood. Yet instead of succumbing to our immune cells, the flukes can dwell in the bloodstream for many years. The fluke’s outer surface, or tegument, is key to its success as a long-lived parasite. The tegument clothes the entire adult fluke and hides its most vulnerable tissues from the prying eyes of the immune system. As such, it is us as human hosts (and not the flukes) who are fooled by the parasites’ remarkable “clothes”.
A fluke’s tegument forms an almost impenetrable barrier between the parasite and its host. It also orchestrates an array of processes that allow the fluke to go about its parasitic lifestyle. Many researchers consider the tegument as a rich source of molecules that could be targeted by vaccines and drugs to combat schistosomiasis. Recent studies have revealed a great deal about the molecular composition of the tegument, but we know far less about how the tegument regenerates after it has been damaged Now in eLife, researchers tell a previously untold chapter in this tale of parasitic flatworms – how a population of stem cells continuously rejuvenates the outer surface of a human parasitic flatworm.
Stem cell progeny contribute to the schistosome host-parasite interface. (2016) eLife 5: e12473 doi: 10.7554/eLife.12473
Schistosomes infect more than 200 million of the world’s poorest people. These parasites live in the vasculature, producing eggs that spur a variety of chronic, potentially life-threatening, pathologies exacerbated by the long lifespan of schistosomes, that can thrive in the host for decades. How schistosomes maintain their longevity in this immunologically hostile environment is unknown. Here, we demonstrate that somatic stem cells in Schistosoma mansoni are biased towards generating a population of cells expressing factors associated exclusively with the schistosome host-parasite interface, a structure called the tegument. We show cells expressing these tegumental factors are short-lived and rapidly turned over. We suggest that stem cell-driven renewal of this tegumental lineage represents an important strategy for parasite survival in the context of the host vasculature.