PMID- 22772778
OWN - NLM
STAT- MEDLINE
DCOM- 20121113
LR  - 20211021
IS  - 1432-1211 (Electronic)
IS  - 0093-7711 (Linking)
VI  - 64
IP  - 10
DP  - 2012 Oct
TI  - Quantity of HLA-C surface expression and licensing of KIR2DL+ natural killer 
      cells.
PG  - 739-45
LID - 10.1007/s00251-012-0633-1 [doi]
AB  - Natural killer (NK) cells require interaction of inhibitory surface receptors 
      with human leukocyte antigen (HLA) ligands during development to acquire 
      functional competence in a process termed "licensing." The quantity of HLA 
      required for this process is unknown. Two polymorphisms affecting HLA-C surface 
      expression (rs9264942 and rs67384697) have recently been identified, and shown to 
      influence progression of HIV infection. We typed a cohort of healthy donors for 
      the two HLA-C-related polymorphisms, KIR2DL1 and KIR2DL3, and their respective 
      HLA-C ligands and analyzed how HLA ligands influenced licensing status of killer 
      cell immunoglobulin-like receptor (KIR)+ NK cells in terms of degranulation and 
      cytokine production in response to HLA-deficient target cells. The presence of 
      respective HLA class I ligands increased the function of KIR2DL1+ and KIR2DL3+ NK 
      cells in a dose-dependent manner. In contrast, neither of the HLA-C-related 
      polymorphisms nor the quantity of cell surface HLA-C had any significant effect 
      on NK cell function. Interestingly, HLA-Cw7-an HLA-C allele with low surface 
      expression-licensed KIR2DL3+ NK cells more strongly than any other KIR2DL3 
      ligand. The quantity of cell surface HLA-C does not appear to influence licensing 
      of NK cells, and the HLA-C-related polymorphisms presumably influence HIV 
      progression through factors unrelated to NK cell education.
FAU - Charoudeh, Hojjatollah Nozad
AU  - Charoudeh HN
AD  - Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, 
      Hebelstrasse 20, 4031, Basel, Switzerland.
FAU - Schmied, Laurent
AU  - Schmied L
FAU - Gonzalez, Asensio
AU  - Gonzalez A
FAU - Terszowski, Grzegorz
AU  - Terszowski G
FAU - Czaja, Karol
AU  - Czaja K
FAU - Schmitter, Karin
AU  - Schmitter K
FAU - Infanti, Laura
AU  - Infanti L
FAU - Buser, Andreas
AU  - Buser A
FAU - Stern, Martin
AU  - Stern M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120707
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (HLA-C Antigens)
RN  - 0 (Ligands)
RN  - 0 (Receptors, KIR)
RN  - 0 (Receptors, KIR2DL1)
RN  - 0 (Receptors, KIR2DL2)
RN  - 0 (Receptors, KIR2DL3)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - DNA/genetics
MH  - Genotype
MH  - HIV Infections
MH  - HLA-C Antigens/*genetics/metabolism
MH  - Humans
MH  - Killer Cells, Natural/cytology/*metabolism
MH  - Leukocytes
MH  - Ligands
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Genetic/genetics
MH  - Receptors, KIR/*genetics/metabolism
MH  - Receptors, KIR2DL1/*genetics/metabolism
MH  - Receptors, KIR2DL2/*genetics/metabolism
MH  - Receptors, KIR2DL3/*genetics/metabolism
EDAT- 2012/07/10 06:00
MHDA- 2012/11/14 06:00
CRDT- 2012/07/10 06:00
PHST- 2012/03/22 00:00 [received]
PHST- 2012/06/16 00:00 [accepted]
PHST- 2012/07/10 06:00 [entrez]
PHST- 2012/07/10 06:00 [pubmed]
PHST- 2012/11/14 06:00 [medline]
AID - 10.1007/s00251-012-0633-1 [doi]
PST - ppublish
SO  - Immunogenetics. 2012 Oct;64(10):739-45. doi: 10.1007/s00251-012-0633-1. Epub 2012 
      Jul 7.