Dexamethazone (Dx) is a synthetic steroid commonly used in treatment of multiple sclerosis (MS) relapses; it has a number of actions on immune cells, but it might also act on the endothelial cells preventing cellular adhesion at this level. We investigated the adhesion of CD4+ and CD8+ T-lymphocytes from healthy controls to in vitro cultured endothelial cells from human umbelical vein (HUVECs) and brain microvessels (HBECs). Endothelial cells were pretreated with Dx, γ-IFN or both prior to adhesion experiments. Adhering cells were evaluated by cytofluorimetric analysis. Endothelial cells supernates were assessed for β2-microglobulin and IL-1β levels. Both CD4+ and CD8+ cells adhesion increased after γ-IFN treatment of endothelial cells; co-stimulation with Dx did not inhibit this adhesion. In comparison with CD4+ and CD8+ percentages on PBMNCs, reduced percentages, expecially for CD4+ cells, were detected after adhesion (probably due to CD4 down regulation), β2-microglobulin levels in the supernates increased after γ- IFN stimulation and Dx was unable to counteract this action at 72 hours. On the other hand, Dx reduced IL-1β levels by HUVECs, also in costimulation with γ-IFN. No detectable levels of IL-1β were released by HBECs. Apart from the IL-1β release by HBECs, we did not detect major district specific differences between HUVECs and HBECs in the response to the applied stimulations.
|Translated title of the contribution||Lymhocyte subsets adhesion to human cerebral endothelial cells: Modulation by γ-IFN and dexamethazone|
|Number of pages||7|
|Journal||Rivista di Neurobiologia|
|Publication status||Published - 1996|
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