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Division of Oncology, Department of Medicine, and the
Division of Immunology and Transplantation Biology, Department of Pediatrics, Stanford University Medical Center, Stanford, CA 94305
Vaccination with naked DNA encoding a specific allergen has been
shown previously to prevent, but not reverse, the development of
allergen-induced airway hyperresponsiveness (AHR). To enhance the
effectiveness of DNA vaccine therapies and make possible the treatment
of established AHR, we developed a DNA vaccination plasmid containing
OVA cDNA fused to IL-18 cDNA. Vaccination of naive mice either with
this fusion DNA construct or with an OVA cDNA-containing plasmid
protected the mice from the subsequent induction of AHR. Protection
from AHR correlated with increased IFN-
production and reduced
OVA-specific IgE production. The protection appeared to be mediated by
IFN- and CD8+ cells because treatment of mice with
neutralizing anti-IFN- mAb or with depleting anti-CD8 mAb
abolished the protective effect. Moreover, vaccination of mice with
preexisting AHR with the OVA-IL-18 fusion DNA, but not with the OVA
cDNA plasmid, reversed established AHR, reduced allergen-specific IL-4,
and increased allergen-specific IFN- production. Thus, combining
IL-18 cDNA with OVA cDNA resulted in a vaccine construct that protected
against the development of AHR, and that was unique among cDNA
constructs in its capacity to reverse established
AHR.
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