Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6

Very late antigens VLA-1, VLA-2, VLA-3, and VLA-6, belonging to the beta 1 subfamily of integrins, have been identified as receptors for different binding domains of laminin (LM). We have detected VLA-6, but not VLA-1 and VLA-2 on a subset (50-70%) of fresh peripheral blood CD3- , CD16+, CD56+ human...

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Format: Online
Language:English
Published: The Rockefeller University Press 1992
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119439/
id pubmed-2119439
recordtype oai_dc
spelling pubmed-21194392008-04-16 Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6 Articles Very late antigens VLA-1, VLA-2, VLA-3, and VLA-6, belonging to the beta 1 subfamily of integrins, have been identified as receptors for different binding domains of laminin (LM). We have detected VLA-6, but not VLA-1 and VLA-2 on a subset (50-70%) of fresh peripheral blood CD3- , CD16+, CD56+ human natural killer (NK) cells by immunofluorimetric and biochemical analysis. Binding assays performed on LM-coated plates showed that 10-15% of NK cells spontaneously adhere to LM, and this adhesion is mediated by VLA-6. Activation of NK cells through CD16 triggering or by phorbol ester results in a rapid increase of adhesion to LM, which is still mediated by VLA-6. The enhanced adhesiveness is not associated with changes in beta 1 LM receptor expression, while it correlates with changes in the phosphorylation status of alpha 6 subunit. The expression of VLA-6 on NK cells and the modulation of its avidity by activating stimuli may be relevant for NK cell migration and tissue location during inflammation or immune response. The Rockefeller University Press 1992-11-01 /pmc/articles/PMC2119439/ /pubmed/1402670 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
title Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
spellingShingle Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
title_short Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
title_full Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
title_fullStr Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
title_full_unstemmed Triggering through CD16 or phorbol esters enhances adhesion of NK cells to laminin via very late antigen 6
title_sort triggering through cd16 or phorbol esters enhances adhesion of nk cells to laminin via very late antigen 6
description Very late antigens VLA-1, VLA-2, VLA-3, and VLA-6, belonging to the beta 1 subfamily of integrins, have been identified as receptors for different binding domains of laminin (LM). We have detected VLA-6, but not VLA-1 and VLA-2 on a subset (50-70%) of fresh peripheral blood CD3- , CD16+, CD56+ human natural killer (NK) cells by immunofluorimetric and biochemical analysis. Binding assays performed on LM-coated plates showed that 10-15% of NK cells spontaneously adhere to LM, and this adhesion is mediated by VLA-6. Activation of NK cells through CD16 triggering or by phorbol ester results in a rapid increase of adhesion to LM, which is still mediated by VLA-6. The enhanced adhesiveness is not associated with changes in beta 1 LM receptor expression, while it correlates with changes in the phosphorylation status of alpha 6 subunit. The expression of VLA-6 on NK cells and the modulation of its avidity by activating stimuli may be relevant for NK cell migration and tissue location during inflammation or immune response.
publisher The Rockefeller University Press
publishDate 1992
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119439/
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