1
However, the role of basophils in allergic airway inflammation is less clear.
2
However, the mechanism underlying T-bet-mediated inhibition of allergic airway inflammation is still unknown.
3
Objective: To determine the regulatory role of T-bet in antigen-induced allergic airway inflammation.
4
These results demonstrate that Gas6 enhances several features of fungal allergic airway disease.
5
Maternal passive immunity regulated allergic airway inflammation in an FcRn-dependent manner.
6
Depletion of Tr1-like cells after primary sensitization exacerbates allergic airway inflammation.
7
These findings support a proinflammatory and proremodeling role for TGF-beta in allergic airway inflammation.
8
Conclusion: In this noninfectious mouse model of allergic asthma, azithromycin attenuated allergic airway inflammation.
9
These results indicate that SKE is a potential therapeutic agent for allergic airway inflammation.
10
Rationale: The effects of ultrafine particle inhalation on allergic airway inflammation are of growing interest.
11
In summary, immunotherapy is probably a useful treatment for selected cases of allergic airway disease.
12
This may partly contribute to the pathogenesis of airways diseases such as allergic airway inflammation.
13
Finally, allergic airway disease induced by SAA and antigen inhalation was unresponsive to Dex treatment.
14
We investigated the role of Gas6 in the development of fungal allergic airway disease in mice.
15
Adoptive transfer of alveolar macrophages derived from Abx-treated mice was sufficient to increase allergic airway inflammation.
16
We hypothesize that statins inhibit allergic airway inflammation and reduce airway hyperreactivity via a mevalonate-dependent mechanism.
