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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004083,
umls-concept:C0014467,
umls-concept:C0017262,
umls-concept:C0021758,
umls-concept:C0024432,
umls-concept:C0033684,
umls-concept:C0035696,
umls-concept:C0039194,
umls-concept:C0078056,
umls-concept:C0185117,
umls-concept:C0214743,
umls-concept:C0221912,
umls-concept:C0332448,
umls-concept:C0443286,
umls-concept:C0681850,
umls-concept:C1550501,
umls-concept:C1706203,
umls-concept:C2349001,
umls-concept:C2697811,
umls-concept:C2911684
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pubmed:issue |
10
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pubmed:dateCreated |
1997-6-2
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pubmed:abstractText |
IL-13, like IL-4, induces up-regulation of vascular cell adhesion molecule-1 (VCAM-1) expression on human endothelial cells in vitro. This may contribute to local accumulation of alpha4beta1+ inflammatory cells, such as eosinophils, macrophages, and T cells. We tested the hypothesis that in human allergic inflammatory reactions in vivo, IL-13 and IL-4 are both involved in VCAM-1/alpha4beta1-dependent recruitment of inflammatory cells. Cryostat cutaneous sections from 13 atopic subjects taken 6, 24, and 48 h after allergen challenge were processed for immunohistochemical staining and in situ hybridization using mAbs and 35S-labeled riboprobes for IL-4 and IL-13. When compared with diluent sites, allergen provoked significant increases in the numbers of cells that were mRNA+ and protein-positive for both IL-13 and IL-4 that were clearly demonstrable at 6 h, peaked at 24 h, and declined by 48 h. Double immunohistochemical staining/in situ hybridization showed that the majority (>60%) of IL-13 mRNA+ signals were colocalized to CD3+ T cells. The numbers of mRNA+ and protein-positive cells for IL-13 significantly correlated with VCAM-1 immunoreactivity on endothelial cells and with total numbers of infiltrating EG2+ eosinophils, CD45RO+ T cells, and CD68+ macrophages, but not elastase-positive neutrophils, at the 6- and 24-h time points. At 6 h, an association was also observed between the numbers of IL-4 mRNA+ or protein product-positive cells and VCAM-1 expression, although this was not statistically significant. These findings suggest that IL-13 may play an important role in recruitment of inflammatory cells to the site of cutaneous allergic inflammatory reaction through VCAM-1/alpha4beta1-dependent mechanisms.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Allergens,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
158
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5050-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9144526-Adult,
pubmed-meshheading:9144526-Allergens,
pubmed-meshheading:9144526-Eosinophils,
pubmed-meshheading:9144526-Female,
pubmed-meshheading:9144526-Gene Expression,
pubmed-meshheading:9144526-Humans,
pubmed-meshheading:9144526-Hypersensitivity,
pubmed-meshheading:9144526-Immunologic Techniques,
pubmed-meshheading:9144526-In Situ Hybridization,
pubmed-meshheading:9144526-Interleukin-13,
pubmed-meshheading:9144526-Interleukin-4,
pubmed-meshheading:9144526-Macrophages,
pubmed-meshheading:9144526-Male,
pubmed-meshheading:9144526-RNA, Messenger,
pubmed-meshheading:9144526-Skin,
pubmed-meshheading:9144526-T-Lymphocytes,
pubmed-meshheading:9144526-Time Factors,
pubmed-meshheading:9144526-Vascular Cell Adhesion Molecule-1
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pubmed:year |
1997
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pubmed:articleTitle |
Associations between IL-13 and IL-4 (mRNA and protein), vascular cell adhesion molecule-1 expression, and the infiltration of eosinophils, macrophages, and T cells in allergen-induced late-phase cutaneous reactions in atopic subjects.
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pubmed:affiliation |
Allergy and Clinical Immunology, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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