Eosinophils and Associated Disorders: From Basic Science to Therapeutic Perspectives

Dear Colleagues,

Eosinophils are both circulating and tissue-resident leukocytes, traditionally regarded as damaging effector cells. Recently, eosinophils have been subdivided into different subpopulations with distinct phenotypes and functions, namely, resident and inflammatory eosinophils. A role for resident eosinophils (rEos) in healthy tissue has been described, including the maintenance of the tissue microenvironment during organ development, along with the modulation of host innate and adaptive immune responses. The other subtype, inflammatory eosinophils (iEos), has been distinguished based on CD62L of membrane expression and is associated with inflammatory responses in patients with severe asthma and nasal polyps. However, growing evidence now reveals a role for eosinophils not only in asthma but also in autoimmune diseases and vasculitis as well as in hypereosinophilic syndromes. Their presence in inflammatory tissues is a hallmark of the type 2 inflammatory response. Eosinophils primed by interleukin (IL)-5, IL-3, granulocyte macrophage colony-stimulating factor (GM-CSF), and eotaxins can express membrane receptors and adhesion molecules involved in activation and tissue migration. Treatment of eosinophilic diseases has traditionally been through nonspecific eosinophil attenuation via the use of glucocorticoids. However, several novel biologic therapies targeting eosinophil maturation factors, such as IL-5 and IL-5R or IL-4/IL-13R, have recently been approved for clinical use. The aim of this Special Issue is to highlight new findings on the physiological and pathophysiological roles of eosinophils in the various pathologies in which they are involved and discuss current and future therapeutic strategies.

Dr. Andrea Matucci
Dr. Alessandra Vultaggio
Guest Editors

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• regulatory eosinophils
• inflammatory eosinophils
• asthma
• EGPA
• hypereosinophilic syndrome
• eosinophils
• esophagitis
• interleukin-5
• type 2 inflammation
• CRSwNP