Virus-specific CD8+ cells can switch to interleukin 5 production and induce airway eosinophilia.
Virus infections of the lung are thought to predispose individuals to asthma, a disease characterized by eosinophil infiltration of the airways. CD8+ T cells are an important part of the host response to virus infection, however, they have no reported role in eosinophil recruitment. We developed a mouse model of virus peptide-stimulated CD8+ T cell immune responses in the lung. We found that bystander CD4+ T helper cell type 2 immune responses to ovalbumin switched the virus peptide-specific CD8+ T cells in the lung to interleukin (IL) 5 production. Furthermore, when such IL-5-producing CD8 T cells were challenged via the airways with virus peptide, a significant eosinophil infiltration was induced. In vitro studies indicated that IL-4 could switch the virus-specific CD8+ T cells to IL-5 production. These results could explain the link between virus infection and acute exacerbation of asthma and, perhaps more importantly, they indicate an IL-4-dependent mechanism that would impair CD8+ T cell responses and delay viral clearance from the host.
Coyle
A J
AJ
Department of Asthma and Allergy, CIBA-GEIGY Ltd., Basel, Switzerland.
Erard
F
F
Bertrand
C
C
Walti
S
S
Pircher
H
H
Le Gros
G
G
D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D004802:Eosinophilia / Q000209:etiology*; D007114:Immunization; D015847:Interleukin-4 / Q000502:physiology; D015848:Interleukin-5 / Q000096:biosynthesis*; D008168:Lung / Q000276:immunology*; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D015848:Interleukin-5; D015847:Interleukin-4; D010047:Ovalbumin