Helicobacter pylori (Hp) is the causative agent of a variety gastric diseases such as peptic ulcers and chronic gastritis and is implicated as a risk factor in gastric cancer. These diseases are mediated by Hp virulence factors including vacuolating cytotoxin (VacA), which inhibits major histocompatibility complex class II mediated antigen presentation through its effect on the invariant chain dependent pathway and can induce apoptosis in epithelial cells. VacA is assumed to play a pivotal role in establishing chronic Hp infections, potentially though an effect on T cells, but the biochemical pathways in this process have been unclear. In the August 22 Science, Bettina Gebert and colleagues at the Max von Pettenkofer-Institut show that VacA inhibits proliferation of T cells through the T-cell receptor/interleukin-2 (IL-2) signaling pathway (Science, 301:1099-1102, August 22, 2003).