Li Xiaoguang, Ishii Norito, Ohata Chika, Furumura Minao, Hashimoto Takashi
Department of Dermatology, Kurume University School of Medicine and Kurume University Institute of Cutaneous Cell Biology, Kurume, Fukuoka, Japan.
Exp Dermatol. 2014 Mar;23(3):155-6. doi: 10.1111/exd.12317.
Acantholysis in pemphigus vulgaris is induced by binding of autoantibodies to desmoglein 3 (Dsg3). The roles of signalling pathways on development of acantholysis have recently been extensively studied. In the study by Sayar et al., recently published in Exp Dermatol, epidermal growth factor receptor (EGFR) signalling was activated in both in vivo and in vitro pemphigus vulgaris experimental models. However, while EGFR inhibitors suppressed activity of p38 mitogen-activated protein kinase (p38MAPK) linearly, they suppressed activity of c-Myc and acantholysis in a non-linear, V-shaped relationship. These findings indicated complicated interactions among EGFR, p38MAPK and c-Myc in pemphigus vulgaris pathology.
寻常型天疱疮中的棘层松解是由自身抗体与桥粒芯糖蛋白3（Dsg3）结合所诱导的。信号通路在棘层松解发展过程中的作用最近得到了广泛研究。在Sayar等人最近发表于《实验皮肤病学》的研究中，在体内和体外寻常型天疱疮实验模型中，表皮生长因子受体（EGFR）信号均被激活。然而，虽然EGFR抑制剂呈线性抑制p38丝裂原活化蛋白激酶（p38MAPK）的活性，但它们以非线性的V形关系抑制c-Myc的活性和棘层松解。这些发现表明在寻常型天疱疮病理过程中，EGFR、p38MAPK和c-Myc之间存在复杂的相互作用。
