title: The role of human β-defensins in allergic diseases.
abstract: Antimicrobial peptides (AMPs), also referred to as host defence peptides (HDPs), comprise a large family of small molecules broadly distributed throughout the animal and plant kingdom, historically serving as natural antibiotics. In mammals, there are two major families of AMPs/HDPs, the defensins and the cathelicidins. These peptides have evolved to protect against a wide range of infections from bacteria, viruses, fungi and some parasites. However, in addition to their broad-spectrum killing activities, AMPs/HDPs also possess various biological functions. They activate a variety of cell types, such as keratinocytes, airway epithelial cells and mast cells, among others, and regulate cytokine/chemokine production, cell migration, proliferation, differentiation, angiogenesis, the wound healing process and maintenance of the skin barrier function. Recently, it has become clear that alterations in the level of AMPs/HDPs are associated with the initiation and development of various inflammatory and allergic diseases. In this review, we will discuss the regulation and functions of human β-defensins and outline the current evidence supporting the role of these peptides in the pathogenesis of allergic diseases, including atopic dermatitis, allergic rhinitis, asthma and chronic rhinosinusitis. Understanding the functions and mechanisms of human β-defensins may aid in the development of novel therapeutic strategies for allergic diseases.
authors: Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.|Faculty of International Liberal Arts, Juntendo University, Tokyo, Japan.
authors: F
authors: F
authors: Niyonsaba
authors: Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.|Institute of Dermatology, Department of Medical Services, Ministry of Public Health, Bangkok, Thailand.
authors: C
authors: C
authors: Kiatsurayanon
authors: Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
authors: H
authors: H
authors: Ogawa
mesh_terms: D000818:Animals; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D056747:Immunomodulation; D023083:beta-Defensins / Q000378:metabolism*
chemical_list: D023083:beta-Defensins