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10.1126/scitranslmed.aag1370

http://scihub22266oqcxt.onion/10.1126/scitranslmed.aag1370
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C5399547!5399547!27708065
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suck abstract from ncbi


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pmid27708065      Sci+Transl+Med 2016 ; 8 (359): 359ra132
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  • Allergic Asthma is Distinguished by Sensitivity of Allergen-Specific CD4+ T Cells and Airway Structural Cells to Type 2 Inflammation #MMPMID27708065
  • Cho JL; Ling MF; Adams DC; Faustino L; Islam SA; Afshar R; Griffith JW; Harris RS; Ng A; Radicioni G; Ford AA; Han AK; Xavier R; Kwok WW; Boucher R; Moon JJ; Hamilos DL; Kesimer M; Suter MJ; Medoff BD; Luster AD
  • Sci Transl Med 2016[Oct]; 8 (359): 359ra132 PMID27708065show ga
  • Despite systemic sensitization, not all allergic individuals develop asthma symptoms upon airborne allergen exposure. Determination of the factors that lead to the asthma phenotype in allergic individuals could guide treatment and identify novel therapeutic targets. In this study, we utilized segmental allergen challenge (SAC) of allergic asthmatics (AA) and allergic non-asthmatic controls (AC) to determine if there are differences in the airway immune response or airway structural cells that could drive the development of asthma. Both groups developed prominent allergic airway inflammation in response to allergen. However, asthmatic subjects had markedly higher levels of innate type 2 receptors on allergen-specific CD4+ T cells recruited into the airway. There were also increased levels of type 2 cytokines, increased total mucin and increased MUC5AC in response to allergen in the airways of AA subjects. Furthermore, type 2 cytokine levels correlated with the mucin response in AA but not AC subjects, suggesting differences in the airway epithelial response to inflammation. Finally, AA subjects had increased airway smooth muscle mass at baseline measured in vivo using novel orientation-registered optical coherence tomography (OR-OCT). Our data demonstrate that the development of allergic asthma is dependent on the responsiveness of allergen-specific CD4+ T cells to innate type 2 mediators as well as increased sensitivity of airway epithelial cells and smooth muscle to type 2 inflammation.
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