title: Light, including ultraviolet.
abstract: Ultraviolet (UV) light is intricately linked to the functional status of the cutaneous immune system. In susceptible individuals, UV radiation can ignite pathogenic inflammatory pathways leading to allergy or autoimmunity. In others, this same UV radiation can be used as a phototherapy to suppress pathogenic cutaneous immune responses. These vastly different properties are a direct result of UV light's ability to ionize molecules in the skin and thereby chemically alter them. Sometimes these UV-induced chemical reactions are essential, the formation of pre-vitamin D(3) from 7-dehydrocholesterol, for example. In other instances they can be potentially detrimental. UV radiation can ionize a cell's DNA causing adjacent pyrimidine bases to chemically bond to each other. To prevent malignant transformation, a cell may respond to this UV-induced DNA damage by undergoing apoptosis. Although this pathway prevents skin cancer it also has the potential of inducing or exacerbating autoreactive immune responses by exposing the cell's nuclear antigens. Ultraviolet-induced chemical reactions can activate the immune system by a variety of other mechanisms as well. In response to UV irradiation keratinocytes secrete cytokines and chemokines, which activate and recruit leukocytes to the skin. In some individuals UV-induced chemical reactions can synthesize novel antigens resulting in a photoallergy. Alternatively, photosensitizing molecules can damage cells by initiating sunburn-like phototoxic reactions. Herein we review all types of UV-induced skin reactions, especially those involving the immune system.
authors.affiliation: Department of Dermatology, School of Medicine, University of California at Davis, Sacramento, CA 95816, USA. emaverakis@yahoo.com
authors.forename: Emanual
authors.initials: E
authors.lastname: Maverakis
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Miyamura
authors.forename: Michael P
authors.initials: MP
authors.lastname: Bowen
authors.forename: Genevieve
authors.initials: G
authors.lastname: Correa
authors.forename: Yoko
authors.initials: Y
authors.lastname: Ono
authors.forename: Heidi
authors.initials: H
authors.lastname: Goodarzi
mesh_terms: D034961:Antigens, Nuclear / Q000276:immunology; D017209:Apoptosis / Q000276:immunology / Q000528:radiation effects; D001324:Autoantigens / Q000276:immunology; D015551:Autoimmunity / Q000528:radiation effects; D002465:Cell Movement / Q000276:immunology / Q000528:radiation effects; D016207:Cytokines / Q000378:metabolism; D004249:DNA Damage / Q000528:radiation effects; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000517:prevention & control; D007165:Immunosuppression Therapy; D015603:Keratinocytes / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D010787:Photosensitivity Disorders / Q000276:immunology*; D012878:Skin Neoplasms / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D014466:Ultraviolet Rays / Q000009:adverse effects; D014467:Ultraviolet Therapy
chemical_list: D034961:Antigens, Nuclear; D001324:Autoantigens; D016207:Cytokines