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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-3-12
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pubmed:abstractText |
Evidence now suggests that eosinophils and T lymphocytes infiltrating bronchial tissues may play a key role in the pathophysiology of asthma. Circulating eosinophils, lung function, and plasma soluble IL-2 receptor (sIL-2R) were measured in 42 asthmatic patients referred for symptomatic asthma. The patients were divided into two groups based on the presence or absence of atopy. The group of non-atopic asthmatics was further divided according to the patients' requirement for long term oral corticosteroids. The mean sIL-2R +/- s.d. was 36.3 +/- 9.9 pM in the control group, 28.9 +/- 9.2 pM in the atopic asthmatics, 43.3 +/- 18.07 pM in the non-atopic asthmatics without oral steroid therapy, but was increased in the steroid-treated group (62.2 +/- 19.3 pM, P less than 0.01). A significant correlation was found between FEV1 and circulating eosinophils in atopic asthmatics and in non-atopic asthmatics without oral corticosteroid therapy, but not in the steroid-treated group. Furthermore, significant correlations were found between sIL-2R and FEV1, and between sIL-2R and blood eosinophils, in the group of non-atopic asthmatics not on oral steroid therapy. No such correlations were evidenced in the other groups of asthmatics. Similar results were obtained during the clinical course of three non-atopic patients followed for more than 1 year. These data suggest that T cell activation appears more prominent in non-atopic asthma than in atopic asthma. Moreover, it appears that T cell activation can occur in severe forms of asthma despite steroid treatment. Finally, the results suggest a possible link between T cell activation, eosinophils, and lung function, which may reflect a particular pathogenetic mechanism involved in non-atopic asthma.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-1124105,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-1847158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-1970229,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2205142,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2215562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2221594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2252260,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2891886,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-2923380,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-3115640,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-3660304,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-4053332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-5073322,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1735191-6177986
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0009-9104
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
87
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
266-71
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:1735191-Adrenal Cortex Hormones,
pubmed-meshheading:1735191-Asthma,
pubmed-meshheading:1735191-Eosinophils,
pubmed-meshheading:1735191-Forced Expiratory Volume,
pubmed-meshheading:1735191-Humans,
pubmed-meshheading:1735191-Leukocyte Count,
pubmed-meshheading:1735191-Lung,
pubmed-meshheading:1735191-Lymphocyte Activation,
pubmed-meshheading:1735191-Receptors, Interleukin-2,
pubmed-meshheading:1735191-Solubility,
pubmed-meshheading:1735191-T-Lymphocytes
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pubmed:year |
1992
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pubmed:articleTitle |
Levels of soluble IL-2 receptor in plasma from asthmatics. Correlations with blood eosinophilia, lung function, and corticosteroid therapy.
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pubmed:affiliation |
C.J.F. INSERM 90-06, Institut Pasteur, Lille, France.
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pubmed:publicationType |
Journal Article
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