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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1995-2-27
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pubmed:abstractText |
The cutaneous lymphocyte-associated Ag (CLA) is expressed by a subset of circulating memory/effector T cells and by the vast majority of skin-infiltrating T cells. CLA is thought to target skin-associated T cells to inflammatory skin sites by interacting with endothelial cell ligand E-selectin (CD62E). We have examined adhesion molecules involved in the migration of human CLA+ and CLA- memory/effector T lymphocytes through IL-1- and TNF-alpha-activated and nonactivated HUVEC layers under static (nonflow) conditions. CLA-enriched memory/effector T lymphocytes migrated more actively across cytokine-activated HUVEC than CLA-depleted memory/effector T cells. This enhanced migration is dependent on the CLA/E-selectin interaction. mAb to very late Ag-4 (VLA-4) and vascular cell adhesion molecule-1 (VCAM-1) blocked the migration of CLA-enriched, but not of CLA-depleted, T cells across activated HUVEC. The observation that anti-VLA-4 and anti-CLA mAb did not show additional inhibition supports the concept that CLA and VLA-4 are sequentially involved in the extravasation. The fact that only CLA+ T cells were inhibited by the anti-VLA-4 mAb suggests that, in this system, CLA engagement is required for using the VLA-4/VCAM-1 pathway. Our studies demonstrate that CLA+ T cells use LFA-1/intercellular leukocyte adhesion molecule-1 (ICAM-1) for transmigration but that CLA expression is not required for the LFA-1/ICAM-1-dependent transmigration because anti-CD18/CD11a mAbs and anti-ICAM-1 mAbs were able to block T cell migration regardless of the activation state of HUVEC or the CLA expression by T cells. Taken together, our results suggest that CLA has a homing function in conducting the T cell to interact with LFA-1/ICAM-1 and/or VLA-4/VCAM-1; this results in enhanced adhesion and migration across cytokine-activated endothelial cells.
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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/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/CTAGE1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Function-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Very Late Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
|
pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
154
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
1543-50
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:7836740-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:7836740-Antigens, Neoplasm,
pubmed-meshheading:7836740-Cell Movement,
pubmed-meshheading:7836740-Cells, Cultured,
pubmed-meshheading:7836740-Endothelium, Vascular,
pubmed-meshheading:7836740-Humans,
pubmed-meshheading:7836740-Interleukin-1,
pubmed-meshheading:7836740-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:7836740-Membrane Glycoproteins,
pubmed-meshheading:7836740-Receptors, Very Late Antigen,
pubmed-meshheading:7836740-Skin,
pubmed-meshheading:7836740-T-Lymphocyte Subsets,
pubmed-meshheading:7836740-Tumor Necrosis Factor-alpha,
pubmed-meshheading:7836740-Umbilical Veins
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pubmed:year |
1995
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pubmed:articleTitle |
Migration of skin-homing T cells across cytokine-activated human endothelial cell layers involves interaction of the cutaneous lymphocyte-associated antigen (CLA), the very late antigen-4 (VLA-4), and the lymphocyte function-associated antigen-1 (LFA-1).
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pubmed:affiliation |
Swiss Institute of Allergy and Asthma Research, Davos.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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