作者: Chang Ook Park , Seongmin Noh , Shan Jin , Na Ra Lee , Yun Sun Lee
DOI: 10.1111/EXD.12034
关键词: Classical complement pathway 、 Acquired immune system 、 CCL18 、 Innate lymphoid cell 、 Innate immune system 、 Immune system 、 Interleukin 33 、 Immunology 、 Pattern recognition receptor 、 Biology
摘要: Atopic dermatitis (AD) is a highly pruritic, chronic relapsing inflammatory skin disease characterized by innate and adaptive immune reactions. In AD, mechanisms such as pattern recognition receptors antimicrobial peptides have been investigated in detail, but recently, epidermis-derived cytokines, namely thymic stromal lymphopoietin (TSLP), IL-25 IL-33, were shown to participate reactions independently of immunity. addition conventional cells, mast basophils eosinophils, Th2 cytokine-producing invariant natural killer T (iNKT) lymphoid cells (ILCs) Th17/Th22 - iNKT (NK)-like can modulation AD. Accordingly, early control responses AD before activation B that perpetuate inflammation may adequately alleviate acute exacerbations Therefore, we hypothesized select modulators targeting the response could potentially be used for individualized treatment