Because of the IgG effect, however, we cannot conclude that inhibition of the Th2 response is completely protective in this model, since we do observe a small trend for increased elastance in anti-IL-4 treated mice compared to non-inflamed mice.
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The endogenous Th17 response in NO2-promoted allergic airway disease is dispensable for airway hyperresponsiveness and distinct from Th17 adoptive transfer.
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