The Interaction of KIR3DL1*001 with HLA Class I Molecules Is Dependent upon Molecular Microarchitecture within the Bw4 Epitope
Philippa M Saunders, Julian P Vivian, Nikola Baschuk, Travis Beddoe, Jacqueline Widjaja, Geraldine M O'Connor, Corinne Hitchen, Phillip Pymm, Daniel M Andrews, Stephanie Gras, Daniel W McVicar, Jamie Rossjohn, Andrew G Brooks
The Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2015
The killer cell Ig-like receptor 3DL1 (KIR3DL1) inhibits activation of NK cells upon interaction with HLA class I molecules such as HLA-B*57:01, which contains the Bw4 epitope spanning residues 77-83 (e.g., NLRIALR), and not with HLA allomorphs that possess the Bw6 motif (e.g., HLA-B*08:01), which differ at residues 77, 80, 81, 82, and 83. Although Bw4 residues Ile(80) and Arg(83) directly interact with KIR3DL1*001, their precise role in determining KIR3DL1-HLA-Bw4 specificity remains unclear. Recognition of HLA-B*57:01 by either KIR3DL1(+) NK cells or the NK cell line YTS transfected with KIR3DL1*001 was impaired by mutation of residues 80 and 83 of HLA-B*57:01 to the corresponding amino ac..View full abstract
Awarded by Frederick National Laboratory for Cancer Research, National Institutes of Health
Awarded by NATIONAL CANCER INSTITUTE
Awarded by Worldwide Cancer Research
This work was supported by grants from the National Health and Medical Research Council and the Association for International Cancer Research (to A.G.B. and J.R.), and the Intramural Research Program of the National Institutes of Health, National Cancer Institute, National Institute of Allergy and Infectious Diseases, and federal funds from the Frederick National Laboratory for Cancer Research, National Institutes of Health Contract HHSN26120080001E. J.P.V. is an Australian Research Council Discovery Early Career Researcher Award Fellow; D.M.A. is the recipient of a National Health and Medical Research Council Career Development Award; and J.R. is a National Health and Medical Research Council of Australia Fellow.