PMID- 26990677
OWN - NLM
STAT- MEDLINE
DCOM- 20170629
LR  - 20181113
IS  - 1521-4141 (Electronic)
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 46
IP  - 6
DP  - 2016 Jun
TI  - Hematopoietic stem cell transplantation: Improving alloreactive Bw4 donor 
      selection by genotyping codon 86 of KIR3DL1/S1.
PG  - 1511-7
LID - 10.1002/eji.201546236 [doi]
AB  - KIR3DL1 is a natural killer (NK) cell receptor that recognizes the Bw4 epitope of 
      human leukocyte antigen (HLA) class I molecules. Following hematopoietic stem 
      cell transplantation for patients lacking Bw4, KIR3DL1-expressing NK cells from 
      Bw4-positive donors can be alloreactive and eliminate tumor cells. However, 
      KIR3DL1 alleles having T instead of C at nucleotide 320 (encoding leucine 86 
      instead of serine 86) are not expressed on the cell surface. Thus, not all 
      individuals testing positive for KIR3DL1 are optimal donors for Bw4-negative 
      recipients. Therefore, we developed a method for genotyping codon 86, which was 
      validated by its perfect correlation with NK cell phenotype for 100 donors of 
      diverse KIR3DL1/S1 genotype. We typed 600 donors and found that  approximately 12.2% had the 
      KIR3DL1 gene, but did not express cell-surface KIR3DL1. By contrast, 
      high-expressing allotypes were identified when haplotypes from four families with 
      duplicated KIR3DL1/S1 genes were characterized at high resolution. Identifying 
      donors who have KIR3DL1 but lack cell-surface KIR3DL1 would refine donor 
      selection. With this technique, the number of individuals identified who may not 
      be optimal donors for Bw4-negative patients increases by threefold, when compared 
      with standard methods. Taken together, we propose that allele typing of killer 
      cell Ig-like receptor (KIR) polymorphisms should become a standard practice when 
      selecting donors.
CI  - (c) 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
FAU - Alicata, Claudia
AU  - Alicata C
AD  - Dipartimento di Medicina Sperimentale, University of Genoa, Genoa, Italy.
AD  - Centro di Eccellenza per la Ricerca Biomedica, University of Genoa, Genoa, Italy.
FAU - Pende, Daniela
AU  - Pende D
AD  - IRCCS AOU San Martino-IST, Genoa, Italy.
FAU - Meazza, Raffaella
AU  - Meazza R
AD  - IRCCS AOU San Martino-IST, Genoa, Italy.
FAU - Canevali, Paolo
AU  - Canevali P
AD  - Istituto Giannina Gaslini, Genoa, Italy.
FAU - Loiacono, Fabrizio
AU  - Loiacono F
AD  - Istituto Giannina Gaslini, Genoa, Italy.
FAU - Bertaina, Alice
AU  - Bertaina A
AD  - Bambino Gesu Children's Hospital, Rome, Italy.
FAU - Locatelli, Franco
AU  - Locatelli F
AD  - Bambino Gesu Children's Hospital, Rome, Italy.
AD  - Department of Pediatrics, University of Pavia, Italy.
FAU - Nemat-Gorgani, Neda
AU  - Nemat-Gorgani N
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, USA.
FAU - Guethlein, Lisbeth A
AU  - Guethlein LA
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, USA.
FAU - Parham, Peter
AU  - Parham P
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, USA.
AD  - Department of Microbiology and Immunology, Stanford University School of 
      Medicine, Stanford, CA, USA.
FAU - Moretta, Lorenzo
AU  - Moretta L
AD  - Bambino Gesu Children's Hospital, Rome, Italy.
FAU - Moretta, Alessandro
AU  - Moretta A
AD  - Dipartimento di Medicina Sperimentale, University of Genoa, Genoa, Italy.
AD  - Centro di Eccellenza per la Ricerca Biomedica, University of Genoa, Genoa, Italy.
FAU - Bottino, Cristina
AU  - Bottino C
AD  - Dipartimento di Medicina Sperimentale, University of Genoa, Genoa, Italy.
AD  - Istituto Giannina Gaslini, Genoa, Italy.
FAU - Norman, Paul J
AU  - Norman PJ
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, USA.
FAU - Falco, Michela
AU  - Falco M
AD  - Istituto Giannina Gaslini, Genoa, Italy.
LA  - eng
GR  - R01 AI017892/AI/NIAID NIH HHS/United States
GR  - R01 GM109030/GM/NIGMS NIH HHS/United States
GR  - U01 AI090905/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Codon)
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA-Bw4 antigen)
RN  - 0 (KIR3DL1 protein, human)
RN  - 0 (Receptors, KIR3DL1)
RN  - 0 (Receptors, KIR3DS1)
SB  - IM
MH  - Alleles
MH  - Cell Membrane/metabolism
MH  - *Codon
MH  - *Donor Selection
MH  - Gene Expression
MH  - Genotype
MH  - HLA-B Antigens/*immunology
MH  - Haplotypes
MH  - *Hematopoietic Stem Cell Transplantation
MH  - Hematopoietic Stem Cells/*immunology/*metabolism
MH  - Humans
MH  - Killer Cells, Natural/immunology/metabolism
MH  - Models, Biological
MH  - Polymorphism, Single Nucleotide
MH  - Receptors, KIR3DL1/*genetics/metabolism
MH  - Receptors, KIR3DS1/*genetics/metabolism
MH  - Transplantation, Homologous
PMC - PMC5065926
MID - NIHMS821337
OTO - NOTNLM
OT  - Donor selection
OT  - HLA haploidentical hematopoietic stem cell transplantation
OT  - Killer cell Ig-like receptor (KIR)
OT  - Natural killer (NK) cell
OT  - Next-generation sequencing
COIS- DISCLOSURE A. Moretta is founder and shareholder of Innate Pharma (Marseille, 
      France). The remaining authors declare no financial or commercial conflict of 
      interest.
EDAT- 2016/03/19 06:00
MHDA- 2017/07/01 06:00
PMCR- 2017/06/01
CRDT- 2016/03/19 06:00
PHST- 2015/12/04 00:00 [received]
PHST- 2016/02/03 00:00 [revised]
PHST- 2016/03/15 00:00 [accepted]
PHST- 2016/03/19 06:00 [entrez]
PHST- 2016/03/19 06:00 [pubmed]
PHST- 2017/07/01 06:00 [medline]
PHST- 2017/06/01 00:00 [pmc-release]
AID - 10.1002/eji.201546236 [doi]
PST - ppublish
SO  - Eur J Immunol. 2016 Jun;46(6):1511-7. doi: 10.1002/eji.201546236.