Cohn L, Tepper J S, Bottomly K
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520-8011, USA.
J Immunol. 1998 Oct 15;161(8):3813-6.
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.
我们研究了Th1或Th2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鉴定出产生IFN-γ、IL-4和IL-5的CD4 T细胞。在体外产生的TCR转基因Th1或Th2细胞转移并暴露于吸入性抗原后，Th2细胞诱导了AHR和气道嗜酸性粒细胞增多，而Th1细胞诱导了中性粒细胞炎症但无AHR。接下来，为了确定IL-4在Th2细胞诱导的AHR中的精确效应功能，我们将IL-4(-/-) Th2细胞转移到野生型和IL-4(-/-)受体小鼠中。暴露于吸入性抗原后，两组小鼠均表现出AHR，气道嗜酸性粒细胞增多明显减少。因此，Th2细胞产生IL-4对于诱导AHR并非必不可少，但对于嗜酸性粒细胞从肺组织迁移到气道至关重要。
