IL-4 differentiates naive CD8+ T cells to a "Th2-like" phenotype: a link between viral infections and bronchial asthma

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. Neverthe...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1996-10, Vol.796, p.97-103
Main Authors: Coyle, A J, Bertrand, C, Tsuyuki, S, Pircher, H, Walti, S, Le Gros, G, Erard, F
Format: Article
Language:English
Subjects:
AIDS/HIV
Animals
Asthma - etiology
Asthma - metabolism
CD8-Positive T-Lymphocytes - metabolism
Cells, Cultured
Interleukin-4 - metabolism
Lymphocytic choriomeningitis virus
Mice
Mice, Transgenic
Phenotype
Respiratory Tract Infections - complications
Th2 Cells - metabolism
Viral Proteins - pharmacology
Virus Diseases - complications
Virus Diseases - metabolism
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Summary: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.
ISSN:0077-8923
DOI:10.1111/j.1749-6632.1996.tb32571.x