pubmed-article:1710227 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0115305 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0007577 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0078056 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0079717 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0699032 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:1710227 | lifeskim:mentions | umls-concept:C0348080 | lld:lifeskim |
pubmed-article:1710227 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:1710227 | pubmed:dateCreated | 1991-7-5 | lld:pubmed |
pubmed-article:1710227 | pubmed:abstractText | T cell adhesion to endothelium is critical to lymphocyte recirculation and influx into sites of inflammation. We have systematically analyzed the role of four receptor/ligand interactions that mediate adhesion of peripheral human CD4+ T cells to cultured human umbilical vein endothelial cells (HUVEC): T cell LFA-1 binding to ICAM-1 and an alternative ligand ("ICAM-X"), T cell VLA-4 binding to VCAM-1, and T cell binding to ELAM-1. Contributions of these four pathways depend on the activation state of both the T cell and HUVEC, and the differentiation state of the T cell. ELAM-1 plays a significant role in mediating adhesion of resting CD4+ T cells to activated HUVEC. LFA-1 adhesion dominates with PMA-activated T cells but the strength and predominant LFA-1 ligand is determined by the activation state of the HUVEC; while ICAM-1 is the dominant ligand on IL-1-induced HUVEC, "ICAM-X" dominates binding to uninduced HUVEC. Adhesion via VLA-4 depends on induction of its ligand VCAM-1 on activated HUVEC; PMA activation of T cells augments VLA-4-mediated adhesion, both in the model of T/HUVEC binding and in a simplified model of T cell adhesion to VCAM-1-transfected L cells. Unlike LFA-1 and VLA-4, ELAM-1-mediated adhesion is not increased by T cell activation. Differential expression of adhesion molecules on CD4+ T cell subsets understood to be naive and memory cells also regulates T/HUVEC adhesion. Naive T cell adhesion to HUVEC is mediated predominantly by LFA-1 with little or no involvement of the VLA-4 and ELAM-1 pathways. In contrast, memory T cells bind better to HUVEC and utilize all four pathways. These studies demonstrate that there are at least four molecular pathways mediating T/HUVEC adhesion and that the dominance/hierarchy of these pathways varies dramatically with the activation state of the interacting cells and the differentiation state of the T cell. | lld:pubmed |
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pubmed-article:1710227 | pubmed:language | eng | lld:pubmed |
pubmed-article:1710227 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1710227 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1710227 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1710227 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1710227 | pubmed:month | Jun | lld:pubmed |
pubmed-article:1710227 | pubmed:issn | 0021-9525 | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:ShimizuYY | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:ShawSS | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:NewmanWW | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:HorganK JKJ | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:van... | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:BeallL DLD | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:GopalT VTV | lld:pubmed |
pubmed-article:1710227 | pubmed:author | pubmed-author:GraberNN | lld:pubmed |
pubmed-article:1710227 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1710227 | pubmed:volume | 113 | lld:pubmed |
pubmed-article:1710227 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1710227 | pubmed:authorsComplete | Y | lld:pubmed |