摘要
银屑病是一种免疫介导的多基因遗传性皮肤病,其发病机制尚未明确,目前认为可能是遗传、环境和免疫学因素共同作用的结果,在免疫机制方面,白细胞介素(interleukin,IL)-23 /辅助T细胞(helper T cells,Th)17途径已被确定为关键轴,促炎细胞因子IL-17A是其主要作用因子。有研究表明,银屑病患者血清中免疫球蛋白(immune globulin,Ig)E浓度增加。与非病变皮肤相比,病变皮肤有更多的特异性IgE的Fc段高亲和力受体I (receptor I for the Fc region of IgE,FceRI)相关细胞,包括肥大细胞,表皮树突状细胞,朗格汉斯细胞和巨噬细胞,现就银屑病发病机制中IL-17关键轴与IgE的相互作用进行综述。
Psoriasis is an immune-mediated polygenic inherited skin disease.The pathogenesis of psoriasis has not been clarified.It is currently believed that psoriasis may be the result of a combination of genetic,environmental and immunological factors.The interleukin(IL)-23/helper T cells(Th)17 pathway has been identified as a key axis,and the proinflammatory cytokine IL-17A is its main acting factor.Studies have shown that,immunoglobulin(Ig)E in the serum of patients with psoriasis is increased.Compared with non lesion skin,the lesion skin has more specific receptor I for the Fc region of IgE(FceRI)related cells,including mast cells,epidermal dendritic cells,Langerhans cells and macrophages.This review summarized the interaction between IL-17 key axis and IgE in the pathogenesis of psoriasis.
作者
曹雪琛
宋乐彬
鲁严
魏继福
Cao Xuechen;Song Lebin;Lu Yan;Wei Jifu(Department of Dermatology,First Affiliated Hospital of Nanjing Medicine University,Nanjing 210029,China;Department of Pharmacy,First Affiliated Hospital of Nanjing Medicine University,Nanjing 210029,China)
出处
《国际免疫学杂志》
CAS
2021年第1期105-109,共5页
International Journal of Immunology
