PMID- 28695292
OWN - NLM
STAT- MEDLINE
DCOM- 20180827
LR  - 20181113
IS  - 1432-1211 (Electronic)
IS  - 0093-7711 (Print)
IS  - 0093-7711 (Linking)
VI  - 70
IP  - 2
DP  - 2018 Feb
TI  - Specificity of inhibitory KIRs enables NK cells to detect changes in an altered 
      peptide environment.
PG  - 87-97
LID - 10.1007/s00251-017-1019-1 [doi]
AB  - The activity of natural killer (NK) cells is tightly regulated by inhibitory and 
      activating receptors. Inhibitory killer immunoglobulin-like receptors (iKIRs) 
      survey the surface of target cells by monitoring the expression of human 
      leukocyte antigen (HLA) class I. The binding of iKIRs has been shown to be 
      sensitive to the peptides presented by HLA class I, implying that iKIRs have the 
      ability to detect the changes in the repertoire of peptide-HLA class I complexes 
      (pHLA), a process occurring during viral infection and in tumor cells. To study 
      how the pHLA repertoire changes upon infection, and whether an iKIR is able to 
      detect these changes, we study peptides eluted from cells prior and after 
      infection with measles virus (MV). Remarkably, most changes in the repertoire of 
      potential iKIR ligands are predicted to be caused by the altered expression of 
      self-peptides. We show that an iKIR can detect these changes in the presented 
      peptides only if it is sufficiently specific, e.g., if iKIRs can distinguish 
      between different amino acids in the contact residues (e.g., position 7 and 8). 
      Our analysis further indicates that one single iKIR per host is not sufficient to 
      detect changes in the peptide repertoire, suggesting that a multigene family 
      encoding for different iKIRs is required for successful peptide recognition.
FAU - Carrillo-Bustamante, Paola
AU  - Carrillo-Bustamante P
AD  - Theoretical Biology and Bioinformatics, Department of Biology, Utrecht 
      University, Utrecht, The Netherlands. 
      paola.carrillo-bustamante@bioquant.uni-heidelberg.de.
AD  - Center for Modeling and Simulation in the Biosciences (BIOMS/IWR), Max Planck 
      Institute, Heidelberg, Germany. 
      paola.carrillo-bustamante@bioquant.uni-heidelberg.de.
FAU - de Boer, Rob J
AU  - de Boer RJ
AD  - Theoretical Biology and Bioinformatics, Department of Biology, Utrecht 
      University, Utrecht, The Netherlands.
FAU - Kesmir, Can
AU  - Kesmir C
AD  - Theoretical Biology and Bioinformatics, Department of Biology, Utrecht 
      University, Utrecht, The Netherlands.
LA  - eng
GR  - 635.100.025/Nederlandse Organisatie voor Wetenschappelijk Onderzoek 
      (NL)/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170710
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (Amino Acids)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Ligands)
RN  - 0 (Peptides)
RN  - 0 (Receptors, KIR)
SB  - IM
MH  - Amino Acids
MH  - Computer Simulation
MH  - Histocompatibility Antigens Class I/immunology
MH  - Humans
MH  - Killer Cells, Natural/*immunology/*metabolism
MH  - Ligands
MH  - Measles virus/immunology
MH  - Peptides/immunology
MH  - Receptors, KIR/*genetics/metabolism
PMC - PMC5775373
OTO - NOTNLM
OT  - KIR
OT  - NK cells
OT  - Peptide sensitivity
OT  - Viral infection
EDAT- 2017/07/12 06:00
MHDA- 2018/08/28 06:00
PMCR- 2017/07/10
CRDT- 2017/07/12 06:00
PHST- 2016/10/26 00:00 [received]
PHST- 2017/06/20 00:00 [accepted]
PHST- 2017/07/12 06:00 [pubmed]
PHST- 2018/08/28 06:00 [medline]
PHST- 2017/07/12 06:00 [entrez]
PHST- 2017/07/10 00:00 [pmc-release]
AID - 10.1007/s00251-017-1019-1 [pii]
AID - 1019 [pii]
AID - 10.1007/s00251-017-1019-1 [doi]
PST - ppublish
SO  - Immunogenetics. 2018 Feb;70(2):87-97. doi: 10.1007/s00251-017-1019-1. Epub 2017 
      Jul 10.