English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Interleukin-1 Receptor Type II (IL-1RII) is the decoy receptor of IL-1 cytokines. It down-regulates the immune signalling pathways. There is a competitive behaviour between the IL-1RII and IL-1RI, which is the signalling receptor of the IL-1Rs family. By adopting similarities in structure and specific shared ligands, the two receptors are competing regulators of the immune response. Conformational changes of IL-1RII is a crucial factor in its ligand binding and activation. In addition, dynamics and functionality of the receptor are known to be regulated by glycosylation. Herein, all-atom Molecular Dynamics (MD) simulations were carried out to investigate the dynamics of the apo and cytokine-bound IL-1RII upon full glycosylation. Simulations showed that the IL-1RII presents two extended/active and compact/inactive conformations. Glycosylation maintains the conformation in the extended/active state. Furthermore, It was shown that IL-1 cytokine binding to IL-1RII contributes to stabilisation of the receptor. Comparison of IL-1RI and IL-1RII interaction with IL-1 β  at the equilibrium condition predicted that glycosylation could increase the binding possibility of IL-1RII towards its ligand. That supports preservation of the active/extended conformation by glycosylation as observed in MD simulations.

Molecular mechanism of glycosylated IL-1RII counteraction with IL-1RI in regulation of the immune response