Ohtomo Takayuki, Kaminuma Osamu, Kitamura Noriko, Suko Matsunobu, Kobayashi Noriaki, Mori Akio
National Hospital Organization, Sagamihara National Hospital, Clinical Research Center for Allergy and Rheumatology, Sagamihara, Japan.
Int Arch Allergy Immunol. 2009;149 Suppl 1:2-6. doi: 10.1159/000210646. Epub 2009 Jun 3.
Helper T (Th) cells are deeply involved in the pathophysiology of bronchial asthma, such as eosinophilic inflammation, bronchial hyperresponsiveness and remodeling. However, it is still unclear how Th cells contribute to airflow limitation, another cardinal feature of bronchial asthma.
Unprimed BALB/c mice were transferred with ovalbumin (OVA)-reactive Th clones. Pulmonary function was monitored using a Buxco BioSystem Plethysmograph before and after OVA challenge.
When Th-transferred mice were challenged with OVA, enhanced pause (P(enh)), an indicator of airflow limitation was significantly increased 6 and 24 h after challenge, while no response was observed 30 min after challenge. Neither bovine serum albumin, an irrelevant antigen, challenge on Th-transferred mice nor OVA challenge on Th-non-transferred mice caused airway responses.
Th cells conferred antigen-induced airflow limitation to unprimed mice.
辅助性T(Th)细胞深度参与支气管哮喘的病理生理学过程,如嗜酸性粒细胞炎症、支气管高反应性和重塑。然而,Th细胞如何导致气流受限(支气管哮喘的另一个主要特征)仍不清楚。
将卵清蛋白(OVA)反应性Th克隆转移至未致敏的BALB/c小鼠。在OVA激发前后,使用Buxco生物系统体积描记仪监测肺功能。
当用OVA激发Th细胞转移的小鼠时,气流受限指标增强停顿(P(enh))在激发后6小时和24小时显著增加,而在激发后30分钟未观察到反应。对Th细胞转移的小鼠进行无关抗原牛血清白蛋白激发或对未转移Th细胞的小鼠进行OVA激发均未引起气道反应。
Th细胞赋予未致敏小鼠抗原诱导的气流受限。