Interestingly, despite the higher susceptibility of Il17−/− and Tcrδ−/− animals after low- and high-dose infection, a compensatory expansion of other IL-17-producing lymphocytes, such as NKT and MAIT cells,34 (C. Paget, Personal communication) might have contributed to a lower bacterial burden in Tcrδ−/− animals (Fig. 5i). The gene discussed is IL17A; the disease is infection.