Saa3 expression following antigen challenge in NO2-promoted allergic airway disease, we observed a significant diminution of Saa3 expression in allergically sensitized and challenged IL-1R mice compared to WT mice, indicating that Saa3 expression is not required for AHR development and suggesting that SAA3 was not responsible for exacerbated AHR in IL-1R mice. We have previously reported that activation in the airway epithelium of the transcription factor NF-��B is not required for the development of AHR despite potently modulating airway inflammation. These results suggest that mechanisms driving AHR exist that are independent of conventional immune-mediated inflammation. Although not studied by us, alterations in neural signaling provide another potential nonimmune regulatory system controlling smooth muscle contractility. In addition, certain mouse strains have been demonstrated to be more appropriate for measurements of AHR, AbMole Capromorelin tartrate particularly in response to IL-17A, and C57BL/6 mice are amongst the poorest strains in which to study this response. The adoptive transfer of in vitro polarized Th17-cells is a conventional approach to studying the Th17 immune response in vivo and assumes that the inflammatory response following antigen challenge will recapitulate the antigen-specific, endogenously-generated response. This Th17 adoptive transfer model was used to demonstrate the critical nature of Th17 in glucocorticoid-resistant allergic airway disease We therefore sought to compare the in vivo generated immune response in NO2-promoted allergic airway disease to that generated following the adoptive transfer of OVA-specific in vitro polarized Th17 cells. We first observed that the magnitude of the inflammatory response induced following adoptive transfer much greater than that elicited by the endogenous Th17 response in NO2-promoted allergic airway disease. It has been reported that the adoptive transfer of Th17 in vitro polarized D011.10 cells are capable of inducing the production of IL-13 following antigen challenge in vivo. The cytokine induction upon restimulation of lung cells in the presence of OVA was between 3-fold to 10-fold for Th17 cytokines following Th17 adoptive transfer and 6-fold to 30-fold higher for Th2 cytokines following Th2 adoptive transfer, indicating that the potential cytokine production in vivo following adoptive transfer is substantially higher in comparison to the endogenously generated Th17 and Th2 responses. This can easily be explained by the fact that OTII cells all express an OVAspecific TCR, and thus every cell is potentially activated, AbMole 11-hydroxy-sugiol whereas the number of OVA-specific CD4+ T cells generated endogenously is much smaller. However, this observation does not address the discrepancies we uncovered in the sensitivity to Dex 
and anakinra between Th17 adoptive transfer and NO2promoted allergic airway disease. For example, we observed no evidence that increasing the in vitro dose of anakinra resulted in further diminution of IL-17A or further suppression by Dex. Considering that anakinra is a competitive antagonist of IL-1R ligand binding, the resistance observed following Th17 adoptive transfer cannot be explained by magnitude alone. In agreement with previous reports, we observed that IL-17 production ex vivo by lung cells following Th17 adoptive transfer and antigen challenge was resistant to inhibition by Dex, whereas IL-17 production by lung cells from mice sensitized by NO2 was Dex-sensitive. This distinction demonstrates substantial differences in the behavior of the Th17 response between these models.