Chronic spontaneous urticaria (CSU) is considered to be primarily a mast cell–driven disease. However, recent evidence suggests that eosinophils may also have an axial role in symptomology. Histologic studies have demonstrated the presence of both eosinophils and eosinophil granules, indicative of activation, in CSU lesions. Although many allergic and inflammatory conditions are associated with a peripheral blood eosinophilia, the converse appears to be the case in CSU, with a peripheral blood eosinopenia being observed in many patients. Possible mechanisms include the depletion of blood eosinophils by recruitment into the skin during active disease and immunologic destruction in the blood. We also address in some detail the interactions between eosinophils and mast cells, particularly the cytokine cross-talk of these cells and mediator release possibly leading to clinical symptoms. Also, activation by eosinophil proteins of the coagulation pathway leads to the generation of thrombin and increased mast cell degranulation. Finally, treatments aimed at reducing eosinophil accumulation and activation, such as the anti–IL-5 antibodies mepolizumab, reslizumab, and benralizumab, have been reported to reduce CSU symptoms. Clearly, a new picture of an important role of eosinophils in the pathogenesis of CSU is emerging.

慢性自发性荨麻疹（CSU）被认为是主要由肥大细胞引起的疾病。然而，最近的证据表明，嗜酸性粒细胞也可能在症状学中具有轴向作用。组织学研究表明，在CSU病变中同时存在嗜酸性粒细胞和嗜酸性粒细胞颗粒，表明其活化。尽管许多变应性和炎症性疾病与外周血嗜酸性粒细胞增多有关，但在CSU中似乎是相反的情况，在许多患者中都观察到外周血嗜酸性粒细胞减少。可能的机制包括在活动性疾病期间通过募集进入皮肤来消耗血液中的嗜酸性粒细胞，以及血液中的免疫破坏。我们还将详细讨论嗜酸性粒细胞与肥大细胞之间的相互作用，特别是这些细胞的细胞因子串扰和介质释放可能导致临床症状。同样，嗜酸性粒细胞蛋白对凝血途径的激活导致凝血酶的产生和肥大细胞脱粒的增加。最后，据报道，旨在减少嗜酸性粒细胞积累和活化的治疗方法，例如抗-IL-5抗体美泊珠单抗，瑞利珠单抗和贝那珠单抗，可减轻CSU症状。显然，正在出现关于嗜酸性粒细胞在CSU发病机理中重要作用的新图景。据报道，reslizumab和benralizumab可减轻CSU症状。显然，正在出现关于嗜酸性粒细胞在CSU发病机理中重要作用的新图景。据报道，reslizumab和benralizumab可减轻CSU症状。显然，正在出现关于嗜酸性粒细胞在CSU发病机理中重要作用的新图景。