Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
复制标题
DOI：
10.1016/j.jaci.2011.03.043
复制
发表时间：
2011-07-01
影响因子：
14.2
通讯作者：
Ying, Sun
中科院分区：
文献类型：
--
作者：
Corrigan, Chris J.;Wang, Wei;Ying, Sun
背景：白细胞介素 - 25（IL - 25）被认为通过促进2型辅助性T细胞（T(H)2）反应参与过敏性炎症。
目的：验证变应原激发是否会增加特应性受试者哮喘支气管黏膜和皮肤真皮中IL - 25及其受体IL - 25R的表达这一假说。
方法：采用连续的单次和双重免疫染色法评估轻度特应性哮喘受试者（n = 10）在吸入变应原激发前和激发后24小时支气管活检组织以及特应性受试者（n = 10）在变应原皮下注射后长达72小时皮肤活检组织中IL - 25和IL - 25R免疫反应细胞的数量和表型。
结果：在基线状态下，两个器官的大多数表皮细胞均表达IL - 25免疫反应性，且激发后未进一步增强。激发前后表皮中IL - 25R免疫反应细胞均很少见。变应原激发与两个器官黏膜下层中IL - 25和IL - 25R免疫反应性显著（P <.01）增加有关。IL - 25免疫反应性与嗜酸性粒细胞、肥大细胞和内皮细胞共定位，而IL - 25R免疫反应性与嗜酸性粒细胞、肥大细胞、内皮细胞和T淋巴细胞共定位。在两个器官中，均观察到IL - 25表达增加与变应原诱导的迟发性临床反应程度之间存在相关性。
结论：变应原激发可诱导致敏特应性受试者哮喘支气管黏膜和真皮中IL - 25及其受体功能性相关的表达增加。在过敏性炎症过程中，除T细胞外，嗜酸性粒细胞、肥大细胞和内皮细胞也是IL - 25的潜在来源和作用靶点。（《过敏与临床免疫学杂志》2011年；128卷：116 - 24页）
Background: IL-25 is thought to participate in allergic inflammation by propagating T(H)2-type responses.Objective: To address the hypothesis that allergen provocation increases expression of IL-25 and its receptor IL-25R in the asthmatic bronchial mucosa and skin dermis of atopic subjects.Methods: Sequential single and double immunostaining was used to evaluate the numbers and phenotypes of IL-25 and IL-25R immunoreactive cells in bronchial biopsies from mild atopic subjects with asthma (n = 10) before and 24 hours after allergen inhalation challenge and skin biopsies from atopic subjects (n = 10) up to 72 hours after allergen subepidermal injection.Results: IL-25 immunoreactivity was expressed by a majority of epidermal cells in both organs at baseline and was not further augmented by challenge. IL-25R immunoreactive cells were rare in the epidermis before or after challenge. Allergen challenge was associated with significantly (P < .01) increased expression of IL-25 and IL-25R immunoreactivity in the submucosa of both organs. IL-25 immunoreactivity colocalized with eosinophils, mast cells, and endothelial cells, whereas IL-25R immunoreactivity colocalized with eosinophils, mast cells, endothelial cells, and T lymphocytes. In both organs, correlations were observed between increases in IL-25 expression and the magnitudes of the late-phase allergen-induced clinical responses.Conclusion: Allergen provocation induces functionally relevant, increased expression of IL-25 and its receptor in the asthmatic bronchial mucosa and dermis of sensitized atopic subjects. In addition to T cells, eosinophils, mast cells, and endothelial cells are potential sources and targets of IL-25 in the course of allergic inflammation. (J Allergy Clin Immunol 2011; 128: 116-24.)