IL1B and Alzheimer disease: In fact, cutaneous keratinocytes are the main sources of these cytokines in the skin, and the increased expression of inflammasome components associated with exposure to S. aureus antigens may lead to an increase in IL-18 and IL-1β in AD patients.66, 114 In fact, CD68+ macrophages produce IL-1β in the dermis of AD patients,98 and increased epidermal expression of this cytokine is observed in AD patients with filaggrin gene mutations.115