alexa Stimulus-specific inhibition of intracellular adhesion molecule-1 gene expression by TGF-beta.
Diabetes & Endocrinology

Diabetes & Endocrinology

Journal of Diabetes & Metabolism

Author(s): Shrikant P, Lee SJ, Kalvakolanu I, Ransohoff RM, Benveniste EN

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Abstract Astrocytes and microglia, the two major glial cells within the central nervous system, can function as immune effector cells upon activation. Intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein involved in extravasation into inflamed tissue and Ag-specific activation of T lymphocytes, can be induced in astrocytes and microglia by numerous stimuli. In this study, we investigated the role of TGF-beta, an immunosuppressive cytokine, in regulating ICAM-1 expression in glial cells. We previously demonstrated that TNF-alpha, IL-1 beta, IFN-gamma, or IFN-gamma plus LPS (IFN-gamma/LPS) can enhance ICAM-1 expression in astrocytes, while microglia express ICAM-1 only in response to IFN-gamma or IFN-gamma/LPS. TGF-beta alone has a minimal effect on constitutive ICAM-1 expression in either astrocytes or microglia, but inhibits, in a time-dependent manner, TNF-alpha- or IL-1 beta-induced ICAM-1 mRNA and protein expression in astrocytes. Interestingly, TGF-beta has no effect on IFN-gamma- or IFN-gamma/LPS-induced ICAM-1 expression in astrocytes or microglia. Inhibition of TNF-alpha- or IL-1 beta-induced ICAM-1 mRNA levels by TGF-beta in astrocytes was not due to degradation of ICAM-1 message, rather, inhibition was mediated at the transcriptional level. Similar results were observed in two human astroglioma cell lines, CRT and STT; TGF-beta inhibited TNF-alpha- and IL-1 beta-induced ICAM-1 expression, but IFN-gamma induction of ICAM-1 was unaffected. These results indicate that TGF-beta suppresses ICAM-1 expression in glial cells in a stimulus-specific manner.
This article was published in J Immunol and referenced in Journal of Diabetes & Metabolism

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