pubmed-article:17471178 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C0004096 | lld:lifeskim |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C0282554 | lld:lifeskim |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:17471178 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:17471178 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:17471178 | pubmed:dateCreated | 2007-7-16 | lld:pubmed |
pubmed-article:17471178 | pubmed:abstractText | Asthma is a chronic and sometimes fatal disease, which affects people of all ages throughout the world. Important hallmarks of asthma are airway inflammation and remodelling, with associated bronchial hyperresponsiveness and variable airflow obstruction. These features are orchestrated by cells of both the innate (eosinophils, neutrophils and mast cells) and the adaptive (T(H)2 T cells) immune system, in concert with structural airway cells. Chemokines are important for the recruitment of both immune and structural cells to the lung, and also for their microlocalisation within the lung tissue. Specific blockade of the responses elicited by chemokines and chemokine receptors responsible for the pathological migration of airway cells could therefore be of great therapeutic interest for the treatment of asthma. | lld:pubmed |
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