| 概要 |
Atopic dermatitis is a common, chronic inflammatory skin disease that is characterized by skin barrier dysfunction, inflammation and intense itch. Although the exact mechanisms behind its pathogenesis... remain unclear, it is evident that the complex interplay among barrier dysfunction, inflammation and itch are critical in its development, progression and chronicity. Barrier-disrupted skin produces thymic stromal lymphopoietin and interleukin (IL)-33 ; these in turn promote skin inflammation characterized by type 2 immune deviation. This inflammation then downregulates the expression of filaggrin in keratinocytes and exacerbates epidermal barrier dysfunction. Furthermore, various itch mediators/pruritogens produced during this inflammatory process can act directly on sensory nerves and cause itch. Based on this understanding of the pathophysiology, many new drugs are being developed, and a new era of treatment is underway. Specifically, anti-IL-4 receptor antibody, anti-IL-31 receptor antibody, and JAK inhibitors are already available for use in clinical practice. Still, however, how to select the optimal drug remains a major challenge. In this review, we summarize the basics and recent advances in our understanding of the pathophysiology of atopic dermatitis, including our recent research findings. In addition, the status of development of new drugs is also outlined.続きを見る
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Mendeley出力
113-3_p045