Journal article
Killer cell immunoglobulin-like receptor 3DL1-mediated recognition of human leukocyte antigen B
Julian P Vivian, Renee C Duncan, Richard Berry, Geraldine M O'Connor, Hugh H Reid, Travis Beddoe, Stephanie Gras, Philippa M Saunders, Maya A Olshina, Jacqueline ML Widjaja, Christopher M Harpur, Jie Lin, Sebastien M Maloveste, David A Price, Bernard AP Lafont, Daniel W McVicar, Craig S Clements, Andrew G Brooks, Jamie Rossjohn
Nature | NATURE PUBLISHING GROUP | Published : 2011
DOI: 10.1038/nature10517
Abstract
Members of the killer cell immunoglobulin-like receptor (KIR) family, a large group of polymorphic receptors expressed on natural killer (NK) cells, recognize particular peptide-laden human leukocyte antigen (pHLA) class I molecules and have a pivotal role in innate immune responses. Allelic variation and extensive polymorphism within the three-domain KIR family (KIR3D, domains D0-D1-D2) affects pHLA binding specificity and is linked to the control of viral replication and the treatment outcome of certain haematological malignancies. Here we describe the structure of a human KIR3DL1 receptor bound to HLA-B*5701 complexed with a self-peptide. KIR3DL1 clamped around the carboxy-terminal end of..
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Awarded by Medical Research Council
Awarded by NATIONAL CANCER INSTITUTE
Awarded by NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
Funding Acknowledgements
We thank the staff at the MX2 beamline of the Australian synchrotron for assistance with data collection. We thank A. Radu Aricescu for the gift of the pHLsec vector. This research was supported by the National Health and Medical Research Council of Australia (NHMRC), the Australian Research Council (ARC) and the Intramural Research Programs of the National Cancer Institute and the National Institute of Allergy and Infectious Diseases, National Institutes of Health. D. W. M. and G.M.O'C. were supported by the Intramural AIDS Targeted Antiviral Program of the National Institutes of Health. J.P.V. is supported by an NHMRC Peter Doherty Research Fellowship; D. A. P. is supported by a Medical Research Council (UK) Senior Clinical Fellowship; B. A. P. L. is supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health; C. S. C. is supported by an ARC QEII Fellowship; J.R. is supported by an ARC Federation Fellowship.