Coyle A J, Bertrand C, Tsuyuki S, Pircher H, Walti S, Le Gros G, Erard F
Department of Asthma and Allergy, CIBA GEIGY AG, Basel, Switzerland.
Ann N Y Acad Sci. 1996 Oct 31;796:97-103. doi: 10.1111/j.1749-6632.1996.tb32571.x.
Viral infections of the lung have been postulated to be a major factor in the etiology of bronchial asthma, a disease characterized by eosinophilic inflammation of the airways. In addition, upper respiratory tract infection in asthmatic individuals results in an exacerbation of the disease. Nevertheless, the mechanisms by which viral infection leads to disease exacerbation are poorly understood. CD8+ T cells play an important role in the host defense responses against viral infection, although to date, there are no reports to suggest that CD8+ T cells play any role in eosinophil recruitment. In the present study, we report that CD8+ T cells activated by either immobilized CD3 mAb or specific antigen can switch to a phenotype that produces Th2 cytokines and secretes less IFN-gamma. Moreover, in vivo, if a lung mucosal Th2 immune response exists, then antigen-specific activation of CD8 cells results in the development of lung eosinophilic inflammation mediated by the secretion of IL-5 from CD8+ T cells. These results may explain the link between viral infections and bronchial asthma, as this IL-4-dependent switch to CD8+ T cells to IL-5 secretion may not only exacerbate asthma by recruiting eosinophils into the lungs, but the impaired IFN-gamma production may also lead to delayed viral clearance.
肺部病毒感染被认为是支气管哮喘病因中的一个主要因素，支气管哮喘是一种以气道嗜酸性粒细胞炎症为特征的疾病。此外，哮喘患者的上呼吸道感染会导致病情加重。然而，病毒感染导致疾病加重的机制尚不清楚。CD8 + T细胞在宿主对抗病毒感染的防御反应中发挥重要作用，尽管迄今为止，尚无报道表明CD8 + T细胞在嗜酸性粒细胞募集中发挥任何作用。在本研究中，我们报告，被固定化CD3单克隆抗体或特异性抗原激活的CD8 + T细胞可转变为产生Th2细胞因子且分泌较少干扰素-γ的表型。此外，在体内，如果存在肺黏膜Th2免疫反应，那么CD8细胞的抗原特异性激活会导致由CD8 + T细胞分泌IL-5介导的肺嗜酸性粒细胞炎症的发展。这些结果可能解释了病毒感染与支气管哮喘之间的联系，因为这种依赖IL-4的CD8 + T细胞向IL-5分泌转变不仅可能通过将嗜酸性粒细胞募集到肺部而加重哮喘，而且干扰素-γ产生受损也可能导致病毒清除延迟。
