IL17A and infection: When we compared the ability of CD28+/+ and CD28−/− γδ T cells to differentiate into cytokine-producing cells, we observed similar percentages and numbers of IL-17A+ and IFNγ+ γδ T cells in both genotypes, regardless of the duration of infection (Figure S2B) or the dose of anti-TCRγδ mAb used to re-stimulate γδ T cell effectors in vitro (Figure 6D and E).