Published online August 1, 2005
PEDIATRICS
Vol. 116
No. 2
August 2005, pp.
557
(doi:10.1542/peds.2005-0698UU)
Viral-Induced T Helper Type 1 Responses Enhance Allergic Disease by Effects on Lung Dendritic Cells
Akaluck Thatayatikom, MD
St Louis, MO
Andrew H. Liu, MD
Denver, CO
Dahl ME, Dabbagh K, Liggitt D, Kim S, Lewis DB. Nat Immunol. 2004;5:337–343
 |
Purpose of the Study.
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To determine the role of interferon (IFN)-
and dendritic cells
in allergic pulmonary disease after influenza A infection.
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Study Population.
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IFN-
knockout and wild-type mice completely recovered from influenza
A infection were studied.
|
Methods.
|
|---|
Mice were inoculated intranasally with influenza A virus. The
postinfluenza mice were then sensitized and challenged with
allergen. Airway inflammatory cells, specific antibody responses,
and pulmonary dendritic cell functions were examined. In some
of the wild-type mice, a neutralizing IFN-
monoclonal antibody
was administered repeatedly after the viral inoculation.
|
Result.
|
|---|
Pulmonary dendritic cells of postinfluenza mice enhanced allergen-specific
T-helper (Th)2 responses via an IFN-
-dependent mechanism.
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Conclusion.
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The Th1 immune response caused by an influenza infection perpetuates
Th2-dependent allergic asthma by altering pulmonary dendritic
cell function.
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Reviewers’ Comments.
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The role of respiratory viral infections in the development
of allergen sensitization and asthma has been perplexing. Acute
viral respiratory tract infections are the primary cause of
asthma exacerbations in children and adults; however, the influence
of viral respiratory infections on subsequent allergic sensitization
and disease in young children is unclear. Viral infections are
simplistically thought to augment Th1 (interleukin [IL]-12 and
IFN-
) responses and, as a result, antagonize Th2 (IL-4, IL-5,
and IL-13) responses and decrease the risk of developing atopic
diseases and asthma (ie, the hygiene hypothesis). Based on mouse
models of allergic asthma, the impact of influenza infection
on Th2 development and allergen sensitization has resulted in
both beneficial and detrimental outcomes. The factors accounting
for the different results are likely to be differences in experimental
methods, including the timing of infections relative to allergen
sensitization, the type and dose of allergen used, and the strain
of the mouse. The findings of the Dahl et al study indicate
that a preceding influenza infection with subsequent Th1 immune
responses can amplify subsequent Th2 immunity. Thus, the Th1-Th2
paradigm of mutual exclusivity (ie, Th1 inhibits Th2, and vice
versa) seems to be overly simplistic in the circumstance in
which Th1 begets Th2. Although the result of the study has not
been observed or correlated in humans, the finding may provide
a mechanistic explanation for a recent report of the increased
risk of asthma/reactive airways disease in young children <36
months of age who received a live attenuated intranasal influenza
vaccine (published by Bergen et al in
Pediatr Infect Dis J.
2004;23:138-144).
PEDIATRICS (ISSN 1098-4275). ©2005 by the American Academy of Pediatrics
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Purpose of the Study.
Study Population.
