The Roles of Th2-Type Cytokines in the Pathogenesis of Atopic Dermatitis

Abstract

Atopic dermatitis (AD) is a chronic, relapsing, highly pruritic inflammatory skin disease (1, 2). Analyses of the cytokine expression profile in skin lesions of AD patients show that the Th2-type immune response is dominant in AD inflammation (3, 4). Interleukin-4 (IL4), IL-5, and IL-13 are signature cytokines of the Th2-type immune response. Expression of IL-4 and IL-13 is significantly high in acute lesions of AD skin; however, it is downregulated in chronic lesions. In contrast, expression of IL-5 is more elevated in chronic lesions than in acute lesions. High expression of IL-4, IL-5, and IL-13 in AD skins leads to high serum levels of IgE and eosinophilia, typical clinical features of AD. In addition to IL-5, expression of interferon-┛ (IFN-┛) and IL-12 is elevated in chronic skin lesions of AD. IFN-┛ and IL-12 are signature cytokines of Th1-type immune response. It has remained unclear why this immune milieu change occurs. Based on observations of the predominant Th2-type immune responses in AD patients, many studies using model mice or involving genetic association have been performed to investigate the role played by Th2-type cytokines in the pathogenesis of AD. It is hoped that Th2-type cytokines will prove to be good targets to develop therapeutic agents for AD. In this chapter, we focus on these topics; we do not review the details of the structures, the signal pathways, or the biological functions of these Th2-type cytokines. Please refer to other articles regarding with these subjects (5-10).