IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells.
IL-4-independent induction of airway hyperresponsiveness by Th2, but not Th1, cells.
复制标题
DOI：
10.4049/jimmunol.161.8.3813
复制
发表时间：
1998-10
影响因子：
4.4
通讯作者：
L. Cohn;J. Tepper;K. Bottomly
中科院分区：
文献类型：
--
作者：
L. Cohn;J. Tepper;K. Bottomly
我们研究了Th 1或Th 2细胞在气道高反应性（AHR）中的作用，因为在哮喘患者的气道中已经鉴定出产生IFN-γ和IL-4和IL-5的CD 4 T细胞。在体外产生的TCR转基因Th 1或Th 2细胞的转移和暴露于吸入Ag后，Th 2细胞诱导AHR和气道嗜酸性粒细胞增多症，而Th 1细胞诱导嗜酸性粒细胞炎症没有AHR。接下来，为了确定IL-4在Th 2细胞诱导的AHR中的精确效应子功能，我们将IL-4（-/-）Th 2细胞转移到野生型和IL-4（-/-）受体小鼠中。暴露于吸入性Ag后，两组小鼠均表现出AHR，气道嗜酸性粒细胞增多症显著减少。因此，由Th 2细胞产生的IL-4对于AHR的诱导不是必需的，但是对于嗜酸性粒细胞从肺组织迁移到气道中是关键的。
We investigated the role of Th1 or Th2 cells in airway hyperresponsiveness (AHR), because both IFN-gamma and IL-4 and IL-5-producing CD4 T cells have been identified in the airways of asthmatics. After transfer of in vitro-generated TCR transgenic Th1 or Th2 cells and exposure to inhaled Ag, Th2 cells induced AHR and airway eosinophilia, whereas Th1 cells induced neutrophilic inflammation without AHR. Next, to determine the precise effector function of IL-4 in Th2 cell-induced AHR, we transferred IL-4(-/-) Th2 cells into wild-type and IL-4(-/-) recipient mice. After exposure to inhaled Ag, both groups of mice exhibited AHR with markedly reduced airway eosinophilia. Thus, IL-4 production by Th2 cells is not essential for the induction of AHR, but is critical for the migration of eosinophils from lung tissue into the airways.