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. 2014 Oct 7;2:108. doi: 10.3389/fped.2014.00108

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Copyright © 2014 Rosenzweig, Lei and Burd.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanism of interleukin-1 (IL-1) receptor antagonist (IL-1RA) blockade. IL-1 is produced in response to hypoxia or Toll-like receptor (TLR) activation. The IL-1 receptor (IL-1R) is comprised of an IL-1R1 subunit and an IL-1R accessory protein (IL-1RAcP). IL-1RA binds IL-1R1 with a higher affinity than IL-1α or IL-1β, but does not recruit IL-1RAcP. Without heterodimerization of the IL-1 receptor complex, no signaling occurs. Binding of IL-1α or IL-1β to IL-1R1 recruits IL-1RAcP and intracellular signaling is initiated, leading to the expression of acute-phase response genes such as IL-1, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). In the brain, these pro-inflammatory cytokines induce neuroinflammation, including neuronal injury and astrogliosis.