- 日本医科大学医学会雑誌 (ISSN:13498975)
- vol.13, no.1, pp.8-21, 2017-02-15 (Released:2017-03-07)
Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease. Both abnormal barrier function and abnormal immune function are closely involved in the etiology of AD. Patients with AD have been subdivided into abnormal filaggrin, normal filaggrin, high immunoglobulin E, normal IgE groups, and so on. Regarding local cytokine profiles in the skin of patients with AD, the involvement of Th2, Th22, and Th17 cells at the acute stage, and the involvement of Th2, Th22, and Th1 cells at the chronic stage have been suggested. The IL-9 level has been reported to be higher in patients with AD than in healthy individuals, but it has also been reported that there are no differences in IL-9 levels between patients with AD and normal individuals. Thus, the role of IL-9 is unclear. The serum IL-18 level is high and induces Th2 reactions in patients with AD. IL-21 is thought to suppress IgE formation, but its activity in relation to AD remains unknown. IL-22 is involved in hyperplasia, increased antimicrobial peptide formation, and reduced filaggrin in patients with AD. IL-25, IL-33, and thymic stromal lymphopoietin are produced in epidermal cells and activate type 2 innate lymphoid cells or premature dendritic cells, resulting in the induction of Th2 reactions. IL-31 is produced by Th2 cells, causing an itching sensation and scratching behavior. A correlation has been reported between serum IL-32 levels and the severity of dermatitis. IL-34 is an element of the control system that suppresses inflammation, but its activity in cases of AD is unknown. One published report describes a correlation between serum IL-37 levels and the severity of dermatitis, but this relationship has not been sufficiently clarified to date, and requires further analysis. In this review, the author has attempted to summarize reports on cytokine expression in patients with AD. The author expects that important cytokines and cells involved in the pathophysiology of AD will be revealed, contributing to strategies for treating AD.