異位性皮膚炎的族群差異及台灣的分子免疫特色

Ethnic Differences of Atopic Dermatitis and Unique Immunopathologic Molecular Signature in Taiwanese

異位性皮膚炎是常見慢性皮膚發炎疾病，主要病理機轉已經確認是表皮障壁缺損以及過度活化的後天免疫第2型發炎反應導致皮膚上過高的第2型炎質表現（第4型介白質與第13型介白質），在慢性的病灶中，也發現了其他發炎物質與發炎細胞浸潤（如第1型、第17型與第22型發炎細胞），但整體詳細疾病成因仍未明瞭，也因此臨床藥物治療成效各異。過去大多數相關研究都著重於西方族群，也就是歐美白種人的免疫特色，治療方針也常以西方族群為主要依據。直到近年來，亞洲族群與台灣的異位性皮膚炎研究嶄露頭角，發現異位性皮膚炎的東亞及台灣族群免疫表現型，與西方族群之免疫表現特色不一。此差異立基於皮膚分析，包括組織學及相關基因表現，顯示皮膚這個標的器官的發炎光譜，也就是異位性皮膚炎主要病理機轉核心，東西方不盡相同。在治療的選擇下，不必然在西方有效或無效的藥物，在東方也能找到相同的趨勢。因此，實際在組織層次上發炎頻譜的異同，才是選擇治療的最適指標，不僅提高治療效率，也落實個人化醫療，保障病人安全，也增加醫療支出的精準，並避免浪費。

Atopic dermatitis (AD) is a common chronic inflammatory skin disease that affects all ethnic groups. Serial studies from both histological and transcriptomic analyses have highlighted the primary pathogenic role of barrier dysfunction and adaptive immune dysregulation in AD, which is centered with aberrant immune activation of type 2 cells that drives overly expressed type 2 cytokines such as IL-4 and IL-13. In chronic disease, the additional contribution from type 1, 17, and 22 cells also secrete many cytokines and recruit cells, resulting in the chronic feature of the disease. The understanding of AD pathogenesis relies mostly on translational analysis from Western population. In this article, we would introduce the recent study progress in Asian and Taiwanese AD populations that obviously are different from Western populations. With an aim to clarify the clinical and molecular heterogeneity of AD from diverse ethnic backgrounds, this report will focus on the alternation of immune axis of AD. By means of illustrating this population-centered analyses from underlying molecular signatures of Asian and Taiwanese AD, we hope to identify the best immune modifying therapies according to the underlying pathogenic pathway to bring excellent therapeutic responses. With the help of the next-generation sequencing technique, precision medicine would not only be focused on choosing specific agents but also specific individuals, and at the same time reduce the global economic burden of the disease.