Dissociation of Innate and Adaptive Immunity by UVB Irradiation

Author:

Kasahara S.1,Wago H.2,Cooper E.L.1

Affiliation:

1. . Laboratory of Comparative Immunology, Department of Neurobiology, UCLA Medical Center, 10833 Le Conte Avenue, Box 951763. Los Angeles, California 90095-1763, USA

2. . Department of Medical Technology, Saitama Medical School Junior College, 38 Morohongo, Moroyamamachi, Iruma-gun, Saitama 350-0495, Japan

Abstract

Increasing ultraviolet-B irradiation (UVB) resulting from diminution of stratospheric ozone is becoming a serious international problem. UVB irradiation exerts not only carcinogenic effects on animals but also causes them to become vulnerable to infections by modulating their immune responses. UVB irradiation suppresses innate immune functions of cells such as macrophages, neutrophils, Langerhans cells, dendritic cells, and the serum component, complement. UVB irradiation also causes changes in cytokine profiles, represented by the induction of a paradigm switch involving Th1/Th2 phenotypes. According to earlier studies, Th1 responses are suppressed, whereas Th2 activities are augmented by UVB irradiation. These immune modulations are caused by several pathways via cytokines and neuropeptides, and eventually may lead to increasing incidences of infection, allergy, and cancer. We have reviewed reports concerning UVB-irradiation induced immune modulation from the viewpoint of risks for human diseases and, in addition, for ecosystems and immunity of lower animals.

Publisher

SAGE Publications

Subject

Pharmacology,Immunology,Immunology and Allergy

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