Imperial College London

ProfessorRosemaryBoyton

Faculty of MedicineDepartment of Infectious Disease

Professor of Immunology and Respiratory Medicine
 
 
 
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Contact

 

r.boyton

 
 
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Location

 

8N22Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Sim:2015:10.1002/eji.201545757,
author = {Sim, M and Stowell, J and Seargent, R and Altmann, D and Long, E and Boyton, RJ},
doi = {10.1002/eji.201545757},
journal = {European Journal of Immunology},
pages = {185--191},
title = {KIR2DL3 and KIR2DL1 show similar impact on licensing ofhuman NK cells},
url = {http://dx.doi.org/10.1002/eji.201545757},
volume = {46},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Killer cell immunoglobulin-like receptor/HLA class I (KIR/HLA-I) combinations are associated withdisease risk, implicating functional roles for NK cells (NKCs) or KIR+ T cells. KIR/HLA-I interactionscan act through inhibition of NKC activation by target cells and NKC licensing for greater intrinsicresponsiveness. We compared licensing conferred by the weaker, HLA-C group 1/KIR2DL3, and thestronger, HLA-C group 2/KIR2DL1, inhibitory combinations. The ‘rheostat model’ predicts weakerlicensing by HLA-C1/KIR2DL3 interactions than HLA-C2/KIR2DL1. We analyzed degranulation inNKC subsets expressing single and multiple receptors for HLA-I. NKG2A had the strongest licensingimpact, while KIR2DL3, KIR2DL1, and KIR3DL1 were weaker, and not significantly different to eachother. Presence of one or two matched HLA-C allotypes did not alter licensing of KIR2DL3+ andKIR2DL1+ NKC. Coexpression of activating KIR2DS1 disarmed KIR2DL3+ and KIR2DL1+ NKC to asimilar extent. KIR3DL1 and NKG2A combined for more enhanced licensing of double positive NKCthan the combination of KIR2DL3 and KIR2DL1. Thus, KIR2DL3 and KIR2DL1 have similar capacityto license NKC, suggesting that inhibitory signal strength and amount of available HLA-C ligands donot correlate with NKC licensing. Altogether, our results show that the basis for disease associationsof HLA-C and KIR2DL likely encompasses factors other than licensing.
AU - Sim,M
AU - Stowell,J
AU - Seargent,R
AU - Altmann,D
AU - Long,E
AU - Boyton,RJ
DO - 10.1002/eji.201545757
EP - 191
PY - 2015///
SN - 1521-4141
SP - 185
TI - KIR2DL3 and KIR2DL1 show similar impact on licensing ofhuman NK cells
T2 - European Journal of Immunology
UR - http://dx.doi.org/10.1002/eji.201545757
UR - http://hdl.handle.net/10044/1/26658
VL - 46
ER -