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The modulation of CD44, VCAM-1 and CD71 expression was analysed by flow cytometry in the 1321N1 astrocytoma cell line in the presence of interleukin-1β (IL1β), tumour necrosis factor-α (TNFα) and 1–40 or 25–35 β-amyloid (Aβ) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFα or IL1β. The presence of Aβ 1–40 fragment, alone or in combination with IL1β, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Aβ 1–40 fragment and of IL1β or TNFα caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Aβ 25–35 fragment was always inactive. These results indicates that Aβ 1–40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that β-amyloid can act as immunological mediator. © 2003 Wiley-Liss, Inc.

The modulation of CD44, VCAM-1 and CD71 expression was analysed by flow cytometry in the 1321N1 astrocytoma cell line in the presence of interleukin-1beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and 1-40 or 25-35 beta-amyloid (Abeta) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFalpha or IL1beta. The presence of Abeta 1-40 fragment, alone or in combination with IL1beta, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Abeta 1-40 fragment and of IL1beta or TNFalpha caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Abeta 25-35 fragment was always inactive. These results indicates that Abeta 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that beta-amyloid can act as immunological mediator.