Fig. 3

Agr-regulated toxins in atopic dermatitis. A Upon contact with S. aureus, keratinocytes detect PSMα, triggering the release of alarming signals, such as IL-1α and IL-36α. The receptors IL-1R and IL-36R become amplified during the inflammatory response in immunocompetent cells, leading to the induction of IL-17-producing γδ T cells and ILC3. IL-17 plays a crucial role in protective immunity against bacteria by promoting neutrophil recruitment. δ-toxin is a potent inducer of mast cell degranulation, contributing to the Th2-driven skin inflammation represented by IgE and IL-4 production. B Once bacteria reach the dermis, S. aureus utilizes PSMα to escape from phagosomes into the cytosol and limit both oxidative and non-oxidative pathogen killing after neutrophil engulfment. This leads to bacterial growth and consecutive inflammation in dermis. PSM: phenol-soluble modulin