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onclusion, our in vivo and in vitro studies presented the evidence that not only Th2 but also Th17 mediated inflammation was involved in the AR pathological mechanism. The Th17 response was reduced in AR following SIT. The relationship between IL10 producing CD4+ T cell and Th17 immunity in AR and its response to SIT needs to be further clarified. The clinical relevance between Th17 and AR suggest
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