| pubmed-article:11686868 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0004096 | lld:lifeskim |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0021759 | lld:lifeskim |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:11686868 | lifeskim:mentions | umls-concept:C0700624 | lld:lifeskim |
| pubmed-article:11686868 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11686868 | pubmed:dateCreated | 2001-11-5 | lld:pubmed |
| pubmed-article:11686868 | pubmed:abstractText | Interleukin-5 is produced by a number of cell types, and is responsible for the maturation and release of eosinophils in the bone marrow. In humans, interleukin-5 is a very selective cytokine as a result of the restricted expression of the interleukin-5 receptor on eosinophils and basophils. Eosinophils are a prominent feature in the pulmonary inflammation that is associated with allergic airway diseases, suggesting that inhibition of interleukin-5 is a viable treatment. The present review addresses the data that relate interleukin-5 to pulmonary inflammation and function in animal models, and the use of neutralizing anti-interleukin-5 monoclonal antibodies for the treatment of asthma in humans. | lld:pubmed |
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| pubmed-article:11686868 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11686868 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11686868 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11686868 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
