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Division of Immunology and Transplantation Biology, Departments of Pediatrics and
Pathology, Stanford University, Stanford, CA 94305
Viral respiratory infections have been implicated in influencing
allergen sensitization and the development of asthma, but their exact
role remains controversial. Because respiratory exposure to Ag normally
engenders T cell tolerance and prevents the development of airway
hyperreactivity (AHR) and inflammation, we examined the effects of
influenza A virus infection on tolerance induced by exposure to
intranasal (i.n.) OVA and the subsequent development of AHR. We found
that concurrent infection with influenza A abrogated tolerance induced
by exposure to i.n. OVA, and instead led to the development of AHR
accompanied by the production of OVA-specific IgE, IL-4, IL-5, IL-13,
and IFN-
. When both IL-4 and IL-5 were neutralized in this system,
AHR was still induced, suggesting that influenza-induced cytokines such
as IL-13, or mechanisms unrelated to cytokines, might be responsible
for the development of AHR. The length of time between influenza A
infection and i.n. exposure to OVA was crucial, because mice exposed to
i.n. OVA 15–30 days after viral inoculation developed neither AHR nor
OVA-specific tolerance. These mice instead acquired Th1-biased
OVA-specific immune responses associated with vigorous OVA-induced T
cell proliferation, and reduced production of OVA-specific IgE. The
protective effect of influenza A on AHR was dependent on IFN-,
because protection was abrogated with a neutralizing anti-IFN-
mAb. These results suggest that viral respiratory infection interferes
with the development of respiratory allergen-induced tolerance, and
that the time interval between viral infection and allergen exposure is
critical in determining whether viral infection will enhance, or
protect against, the development of respiratory allergen sensitization
and AHR.
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