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.