| pubmed-article:9124376 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0123771 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0597750 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
| pubmed-article:9124376 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:9124376 | pubmed:issue | 2 Pt 1 | lld:pubmed |
| pubmed-article:9124376 | pubmed:dateCreated | 1997-4-24 | lld:pubmed |
| pubmed-article:9124376 | pubmed:abstractText | The functional role of interleukin (IL)-4 in the development of airway hyperresponsiveness (AHR) and pulmonary eosinophilia in response to sensitization and challenge of mice with sheep red blood cells (SRBC) was examined. Control- and SRBC-sensitized A/J mice were treated with an antibody to the murine IL-4 receptor (anti-IL-4R) 3 days before intratracheal challenge with the antigen or vehicle only. Blockade of IL-4R significantly reduced antigen-induced AHR and prevented increases in goblet cells and bronchoalveolar lavage (BAL) eosinophils. Treatment with anti-IL-4R did not affect antigen-induced increases in lung mRNA and BAL protein levels of IL-5 and interferon-gamma or IL-4 mRNA but did significantly increase IL-4 protein levels. Antigen-induced AHR was not reduced by treatment with antibodies to the adhesion molecules, vascular cell adhesion molecule-1 and very late activation antigen-4. Administration of IL-4 over a 7-day period did not increase airway reactivity or induce any changes in BAL cell numbers in naive mice. These results demonstrate that IL-4 is necessary for in vivo development of antigen-induced AHR, goblet cell metaplasia, and pulmonary eosinophilia. | lld:pubmed |
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| pubmed-article:9124376 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9124376 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9124376 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9124376 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9124376 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:FinkelmanF... | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:SchofieldB... | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:GavettS HSH | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:Wills-KarpMM | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:KarpC LCL | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:O'HearnD JDJ | lld:pubmed |
| pubmed-article:9124376 | pubmed:author | pubmed-author:PatelE AEA | lld:pubmed |
| pubmed-article:9124376 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9124376 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9124376 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9124376 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9124376 | pubmed:pagination | L253-61 | lld:pubmed |
| pubmed-article:9124376 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9124376 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9124376 | pubmed:articleTitle | Interleukin-4 receptor blockade prevents airway responses induced by antigen challenge in mice. | lld:pubmed |
| pubmed-article:9124376 | pubmed:affiliation | Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205, USA. | lld:pubmed |
| pubmed-article:9124376 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9124376 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9124376 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:16190 | entrezgene:pubmed | pubmed-article:9124376 | lld:entrezgene |
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