For example, in the mouse model of S. aureus skin and soft tissue infection, NLRP3 activity regulates IL-17 production by γδT cells and is protective for the host [29]; in the mouse model of MRSA pneumonia, NLRP3 suppresses bactericidal activities of macrophages and is detrimental for the host [25]; while in the mouse model of acute central nervous system MRSA infection, NLRP3 is dispensable as it can be replaced with AIM2 (absent in melanoma 2) in the IL-1β processing inflammasome complex [30]. This evidence concerns the gene IL1B and infection.