NLRC4 and infection: Consistent with a role for ExoS rather than ExoT in licensing NLRP3 rather than NLRC4 usage, IL-1β secretion by neutrophils infected with ∆exoT mutants (ExoS expressing) was dependent on NLRP3, whereas IL-1β secretion following infection with ∆exoS mutants (ExoT expressing) was not inhibited by MCC950 (Fig. S2G, H).