A protein secreted by parasitic worms can block immune cells from promoting inflammation, a finding of possible therapeutic value for such inflammatory bowel diseases (IBD) as Crohn's and ulcerative colitis. The study by researchers at Edinburgh and Glasgow universities, “A structurally distinct TGF-β mimic from an intestinal helminth parasite potently induces regulatory T cells,” was published in the journal Nature Communications. IBD is characterized by chronic inflammation caused by poor regulation of pro-inflammatory signals produced by immune cells. It is known that bacteria are important regulators of bowel activity, and in maintaining a natural balance of immune responses in the bowel. Such immune-regulation activity is not only restricted to bacteria, with studies having also shown that fungi may play a role in IBD. Previously, researchers found that infection by Heligmosomoides polygyrus, a helminth or worm parasite, could change the natural bacterial balance in the gut in a way that would prevent inflammatory signals in the bowel. The Edinburgh research team found that these parasites produce a protein that is very similar to human transforming growth factor-beta, or TGF-β. This human protein is known to activate regulatory T-cells (Tregs), a subset of immune cells that keep reactive T-cells under control. "Discovering a new protein that can potently induce regulatory T cells (Tregs) from human cells is unexpected and very exciting in terms of finding a new potential biologic for inflammation conditions," Danielle Smyth, the study's lead author, said in a Glasgow University news release. "We hope to explore this option and see whether the Tregs our parasite molecule induce offer a regulatory advantage over current treatments,"