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.
Cover
Timothy L
TL
Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. timothy.l.cover@vanderbilt.edu
D000818:Animals; D001426:Bacterial Proteins / Q000378:metabolism*; D018821:CD18 Antigens / Q000378:metabolism*; D016480:Helicobacter pylori / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D051379:Mice; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism*; D013601:T-Lymphocytes / Q000821:virology*
D001426:Bacterial Proteins; D018821:CD18 Antigens; D011948:Receptors, Antigen, T-Cell; C074689:VacA protein, Helicobacter pylori