| http://purl.uniprot.org/citations/20581095 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20581095 | http://www.w3.org/2000/01/rdf-schema#comment | "Activation of NF-κB in airway epithelium is observed in allergic asthma and is induced by inhalation of numerous infectious and reactive substances. Many of the substances that activate NF-κB in the airway epithelium are also capable of acting as adjuvants to elicit antigen-specific sensitization to concomitantly inhaled protein, thereby circumventing the inherent bias of the lung to promote tolerance to innocuous antigens. We have used a transgenic mouse inducibly expressing a constitutively active mutant of the inhibitor of nuclear factor κB (IκB) kinase β ((CA)IKKβ) that activates NF-κB only in nonciliated airway epithelial cells to test whether activation of this intracellular signaling pathway in this specific cell type is sufficient to establish a pulmonary environment permissive to the development of allergic sensitization to inhaled protein. When airway epithelial (CA)IKKβ was transiently expressed in antigen-naive mice only during initial inhalation of ovalbumin, the mice became allergically sensitized to the antigen. As a consequence, subsequent inhalation of ovalbumin alone led to an allergic asthma-like response that included airway hyperresponsiveness to methacholine, eosinophilia, mucus expression, elevated serum levels of antigen-specific IgE and IgG1, and splenic CD4(+) T cells that secreted T helper type 2 and type 17 cytokines in response to in vitro antigen restimulation. Furthermore, CD11c(+) cells in the mediastinal lymph nodes (MLN) of (CA)IKKβ-expressing mice displayed significantly elevated levels of activation markers. These data implicate airway epithelial NF-κB activation as a critical modulator of the adaptive immune response to inhaled antigens via the secretion of soluble mediators that affect the capacity of CD11c(+) cells to undergo maturation and promote antigen-specific allergic responses."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.org/dc/terms/identifier | "doi:10.1165/rcmb.2010-0106oc"xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/author | "Janssen-Heininger Y.M."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/author | "Poynter M.E."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/author | "Ather J.L."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/author | "Hodgkins S.R."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/name | "Am J Respir Cell Mol Biol"xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/pages | "631-638"xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/title | "Airway epithelial NF-kappaB activation promotes allergic sensitization to an innocuous inhaled antigen."xsd:string |
| http://purl.uniprot.org/citations/20581095 | http://purl.uniprot.org/core/volume | "44"xsd:string |
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