The prolonged survival of eosinophils in skin lesional sites is due to increased IL-5 expression by macrophages during the transition from acute to chronic AD and secretion of autocrine factors inhibiting eosinophil cell apoptosis.[39, 40] Their role has been widely investigated in the cutaneous late-phase reaction (LPR) to allergens; studies in humans have demonstrated that systemic therapy with anti-IL-5 reduces eosinophilia. Here, IL5 is linked to Alzheimer disease.