We identified IL-1α but not IL-1β, most likely released from dying neutrophils, is a key driver of the vicious cycle of inflammation in Ccr2−/− mice, leading to the formation of abscess-like neutrophil clusters in the skin lesion, in contrast to the case of the abscess formation during Staphylococcus aureus infection where IL-1β plays a critical role37. This evidence concerns the gene CCR2 and abscess.