Beta2 integrin mediates entry of a bacterial toxin into T lymphocytes

Helicobacter pylori secretes a pore-forming toxin, VacA, that can cause numerous alterations in gastric epithelial cells and T lymphocytes. In this issue of Cell Host & Microbe, Sewald and colleagues report that beta2 integrin (CD18) mediates entry of VacA into human T cells. Downregulation of T cell responses by VacA may allow H. pylori to evade the adaptive immune response and establish persistent infection.