To determine whether CD28 costimulation is required for in vivo γδ T cell effector functions, we infected CD28+/+ and CD28−/− mice with Listeria monocytogenes, a model pathogen that not only induces IL-17A- and IFNγ-producing γδ T cells [36], [37], but also upregulates the expression of the CD28 ligands, B7.1 and B7.2, on antigen presenting cells early in the course of infection [38–40; data not shown]. This evidence concerns the gene CD86 and infection.