Thus, although recent data established that IL-1β plays a critical component in innate resistance to MTB, the pathways involved in the expression and regulation of IL-1β induction following MTB infection in vivo are complex and may involve mechanisms that do not fit the classical paradigms of TLR recognition and inflammasome-mediated caspase-1 processing seen with other infections or in the response to MTB observed in vitro [130]. Here, IL1B is linked to infection.