■食物过敏的免疫病理学特征在于不受控制的2型免疫应答和特异性IgE产生。最近的研究已经确定,第2组固有淋巴细胞(ILC2)参与食物过敏的致病机制及其严重程度。我们的目的是研究ILC2在非特异性脂质转移蛋白(Prup3)致敏导致的桃子过敏患者中的作用。
■脂质转移蛋白过敏患者和健康对照者外周血单核细胞的免疫反应。我们分析了Prup3对ILC2的摄取,共刺激分子的表达,以及它们在不同实验条件下参与T细胞增殖反应和细胞因子产生:参与第2组固有淋巴细胞活化的细胞因子(IL-33和IL-25),Prup3作为主要的食物过敏原,和两种成分的组合(IL-33/IL-25+Prup3)使用细胞分选,EliSpot,流式细胞术,和共聚焦显微镜。
■我们的结果表明,Prup3过敏原被第2组先天淋巴细胞吸收,根据Prup3的存在及其与IL-33/IL-25的组合来调节它们的共刺激分子表达(CD83和HLA-DR)。Prup3刺激的ILC2以细胞接触依赖性方式在脂质转移蛋白过敏患者中诱导特异性GATA3Th2增殖和细胞因子(IL-4,IL-5和IL-13)产生,而TbetTh1-和FOXP3Treg细胞分化没有变化。
■结果表明,在脂质转移蛋白过敏患者中,负责任的过敏原,Prup3,与第2组先天淋巴样细胞相互作用,促进Th2细胞反应。我们的结果可能在体内感兴趣,因为它们显示了第2组先天淋巴样细胞作为抗原呈递细胞的作用,有助于食物过敏的发展。因此,第2组先天淋巴样细胞可能被认为是潜在的治疗靶点。
UNASSIGNED: Immunopathology in food allergy is characterized by an uncontrolled type 2 immune response and specific-IgE production. Recent studies have determined that group 2 innate lymphoid cells (ILC2) participate in the food allergy pathogenic mechanism and their severity. Our objective was to investigate the role of ILC2 in peach-allergic patients due to non-specific lipid transfer protein (Pru p 3) sensitization.
UNASSIGNED: The immune response in peripheral blood mononuclear cells was characterized in lipid transfer protein-allergic patients and healthy controls. We have analyzed the Pru p 3 uptake on ILC2, the expression of costimulatory molecules, and their involvement on the T-cell proliferative response and cytokine production under different experimental conditions: cytokines involved in group 2 innate lymphoid cell activation (IL-33 and IL-25), Pru p 3 as main food allergen, and the combination of both components (IL-33/IL-25+Pru p 3) using cell sorting, EliSpot, flow cytometry, and confocal microscopy.
UNASSIGNED: Our results show that Pru p 3 allergen is taken up by group 2 innate lymphoid cells, regulating their costimulatory molecule expression (CD83 and HLA-DR) depending on the presence of Pru p 3 and its combination with IL-33/IL-25. The Pru p 3-stimulated ILC2 induced specific GATA3+Th2 proliferation and cytokine (IL-4, IL-5, and IL-13) production in lipid transfer protein-allergic patients in a cell contact-dependent manner with no changes in Tbet+Th1- and FOXP3+Treg cell differentiation.
UNASSIGNED: The results indicate that in lipid transfer protein-allergic patients, the responsible allergen, Pru p 3, interacts with group 2 innate lymphoid cells, promoting a Th2 cell response. Our results might be of interest in vivo, as they show a role of group 2 innate lymphoid cells as antigen-presenting cells, contributing to the development of food allergy. Consequently, group 2 innate lymphoid cells may be considered as potential therapeutic targets.