Balaji, Gautham R., Aguilar, Oscar A., Tanaka, Miho, Shingu-Vazquez, Miguel A., Fu, Zhihui, Gully, Benjamin S., Lanier, Lewis L., Carlyle, James R., Rossjohn, Jamie ORCID: https://orcid.org/0000-0002-2020-7522 and Berry, Richard 2018. Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition. Nature Communications 9 (1) , 4623. 10.1038/s41467-018-06989-2 |
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Abstract
The interaction between natural killer (NK) cell inhibitory receptors and their cognate ligands constitutes a key mechanism by which healthy tissues are protected from NK cell-mediated lysis. However, self-ligand recognition remains poorly understood within the prototypical NKR-P1 receptor family. Here we report the structure of the inhibitory NKR-P1B receptor bound to its cognate host ligand, Clr-b. NKR-P1B and Clr-b interact via a head-to-head docking mode through an interface that includes a large array of polar interactions. NKR-P1B:Clr-b recognition is extremely sensitive to mutations at the heterodimeric interface, with most mutations severely impacting both Clr-b binding and NKR-P1B receptor function to implicate a low affinity interaction. Within the structure, two NKR-P1B:Clr-b complexes are cross-linked by a non-classic NKR-P1B homodimer, and the disruption of homodimer formation abrogates Clr-b recognition. These data provide an insight into a fundamental missing-self recognition system and suggest an avidity-based mechanism underpins NKR-P1B receptor function.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Publisher: | Nature Publishing Group |
ISSN: | 2041-1723 |
Date of First Compliant Deposit: | 20 November 2018 |
Date of Acceptance: | 9 October 2018 |
Last Modified: | 05 May 2023 18:09 |
URI: | https://orca.cardiff.ac.uk/id/eprint/116952 |
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