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Interleukin-1 and IL-1 receptor antagonist in stroke: mechanisms and potential therapeutics

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Inflammation and Stroke

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The IL-1 family comprises two agonists, IL-lα and IL-1β, the products of separate genes, which exert virtually identical actions. Both ligands are produced as precursors; pro-IL-1a is biologically active, but pro-IL-1β is inactive and must be cleaved by the enzyme caspase-1. The mechanisms through which IL-1α and β are released from the cell are unknown. IL-1a appears to remain largely intracellular, whereas IL-1β is released more readily, but has no classical leader sequence. It now seems likely that release of IL-1β is linked directly to cleavage by caspase-1 (see [1]). Recent evidence suggests that these events are regulated by extracellular ATP acting on purinergic P2x7receptors; pharmacological activation of these receptors leads to IL-1β cleavage and release from macrophages and microglia [2, 3>].

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Rothwell, N.J., Loddick, S.A. (2001). Interleukin-1 and IL-1 receptor antagonist in stroke: mechanisms and potential therapeutics. In: Feuerstein, G.Z. (eds) Inflammation and Stroke. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8297-2_14

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  • DOI: https://doi.org/10.1007/978-3-0348-8297-2_14

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9508-8

  • Online ISBN: 978-3-0348-8297-2

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