In the context of S. aureus infection, our colleagues found that while the primary challenge of IL-1β deficient mice led to decreased bacterial clearance, greater lesions, and impaired neutrophil abscess formation, these functions were restored upon secondary infection by LN draining γδ T cells through TLR2/MyD88 signaling to produce IFNγ and TNF [61]. This evidence concerns the gene IL1B and infection.