Immunoallergology Unit, AOU Careggi, University of Florence, Florence.
Translational Immunology Unit, Immunology Area, Pediatric Hospital Bambino Gesù, IRCCS, Rome, Italy.
Curr Opin Allergy Clin Immunol. 2020 Apr;20(2):175-180. doi: 10.1097/ACI.0000000000000614.
Clinical conditions associated with hypereosinophilia represent a field of particular interest, taking into account the epidemiological impact of the different primary and secondary forms. In addition to a classical Th1 response, also Th2 cells can be involved in the pathogenesis of autoimmune diseases, among them eosinophilic forms such as eosinophilic granulomatosis with polyangiitis.
In patients with severe asthma, recent evidence highlights the role of pathogenic autoantibodies against autologous eosinophil proteins (e.g. eosinophil peroxidase) suggest the role of autoimmune mechanisms, particularly in patients in which asthma is included in eosinophilic vasculitis with antineutrophilic autoantibody positivity. Is now evident that in addition to Th2 cells, also type 2 innate lymphoid cells and Th1/Th17 cells play a central role in the pathogenesis of hypereosinophilic syndrome.
The definition of cellular and molecular mechanisms and the critical role of specific cytokines involved in the pathogenesis of hypereosinophilic syndrome open the way to new therapeutic strategies by using biological agents targeting these specific factors.
伴有嗜酸性粒细胞增多的临床病症是一个特别值得关注的领域，这考虑到了不同原发性和继发性疾病的流行病学影响。除了经典的 Th1 反应外，Th2 细胞也可能参与自身免疫性疾病的发病机制，其中包括嗜酸性粒细胞增多症，如嗜酸性肉芽肿伴多血管炎。
在严重哮喘患者中，最近的证据强调了针对自身嗜酸性粒细胞蛋白（如嗜酸性过氧化物酶）的致病性自身抗体的作用，提示自身免疫机制的作用，特别是在哮喘包含抗中性粒细胞自身抗体阳性的嗜酸性血管炎的患者中。现在很明显，除了 Th2 细胞外，2 型先天淋巴细胞和 Th1/Th17 细胞也在嗜酸性粒细胞增多综合征的发病机制中发挥核心作用。
细胞和分子机制的定义以及参与嗜酸性粒细胞增多综合征发病机制的特定细胞因子的关键作用为使用针对这些特定因素的生物制剂开辟了新的治疗策略。
