Lymphocytes in human atherosclerotic plaque exhibit the elastin-laminin receptor: potential role in atherogenesis

The purpose of this immuno-histochemical study was to investigate if lymphocytes, present in the human atherosclerotic plaque, exhibit the elastin-laminin receptor. We showed recently that human activated lymphocytes in vitro express this receptor. Briefly, we demonstrated by immuno-localization exp...

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Veröffentlicht in:Atherosclerosis 1997-11, Vol.135 (1), p.103-107
Hauptverfasser: Péterszegi, G, Mandet, C, Texier, S, Robert, L, Bruneval, P
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Sprache:eng
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Zusammenfassung:The purpose of this immuno-histochemical study was to investigate if lymphocytes, present in the human atherosclerotic plaque, exhibit the elastin-laminin receptor. We showed recently that human activated lymphocytes in vitro express this receptor. Briefly, we demonstrated by immuno-localization experiments and by flow cytometry that this receptor is available on the cell surface of human activated lymphocytes, free to react with ligands and show capping. The activation of this receptor by elastin peptides triggers several cellular reactions of biological interest as shown previously such as chemotactic movement to an elastin peptide gradient, modulation of the biosynthesis of connective tissue macromolecules, increase of protease synthesis and release of free radicals (O 2 −⋅, NO ⋅) from mononuclear and endothelial cells, modifications of ion fluxes and also increase of cell proliferation. All these processes may contribute to the development of the atherosclerotic lesion. Two of the previously demonstrated cell reactions mediated by the receptor could be demonstrated also on PHA-stimulated human lymphocytes namely stimulation of cell proliferation and increase of elastase activity. We demonstrated in the present immuno-histological study that about 50–60% of lymphocytes of the human atherosclerotic plaque obtained by endarterectomy express the 67 kDa subunit of the elastin-laminin receptor confirming that the above described phenomena could contribute to the chronicity of the lesion.
ISSN:0021-9150
1879-1484
DOI:10.1016/S0021-9150(97)00155-X