PMID- 16533882
OWN - NLM
STAT- MEDLINE
DCOM- 20060503
LR  - 20220318
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 203
IP  - 3
DP  - 2006 Mar 20
TI  - Roles for HLA and KIR polymorphisms in natural killer cell repertoire selection 
      and modulation of effector function.
PG  - 633-45
AB  - Interactions between killer cell immunoglobulin-like receptors (KIRs) and human 
      leukocyte antigen (HLA) class I ligands regulate the development and response of 
      human natural killer (NK) cells. Natural selection drove an allele-level group A 
      KIR haplotype and the HLA-C1 ligand to unusually high frequency in the Japanese, 
      who provide a particularly informative population for investigating the 
      mechanisms by which KIR and HLA polymorphism influence NK cell repertoire and 
      function. HLA class I ligands increase the frequencies of NK cells expressing 
      cognate KIR, an effect modified by gene dose, KIR polymorphism, and the presence 
      of other cognate ligand-receptor pairs. The five common Japanese KIR3DLI 
      allotypes have distinguishable inhibitory capacity, frequency of cellular 
      expression, and level of cell surface expression as measured by antibody binding. 
      Although KIR haplotypes encoding 3DL1*001 or 3DL1*005, the strongest inhibitors, 
      have no activating KIR, the dominant haplotype encodes a moderate inhibitor, 
      3DL1*01502, plus functional forms of the activating receptors 2DL4 and 2DS4. In 
      the population, certain combinations of KIR and HLA class I ligand are 
      overrepresented or underrepresented in women, but not men, and thus influence 
      female fitness and survival. These findings show how KIR-HLA interactions shape 
      the genetic and phenotypic KIR repertoires for both individual humans and the 
      population.
FAU - Yawata, Makoto
AU  - Yawata M
AD  - Department of Structural Biology, School of Medicine, Stanford University, 
      Stanford, CA 94305, USA, and Department of Haematology, The Royal Free Hospital, 
      London, UK. myawata@stanford.edu
FAU - Yawata, Nobuyo
AU  - Yawata N
FAU - Draghi, Monia
AU  - Draghi M
FAU - Little, Ann-Margaret
AU  - Little AM
FAU - Partheniou, Fotini
AU  - Partheniou F
FAU - Parham, Peter
AU  - Parham P
LA  - eng
GR  - R01 AI017892/AI/NIAID NIH HHS/United States
GR  - R01 AI022039/AI/NIAID NIH HHS/United States
GR  - AI-017892/AI/NIAID NIH HHS/United States
GR  - AI-022039/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20060313
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (HLA-C Antigens)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, KIR)
RN  - 0 (Receptors, KIR2DL4)
RN  - 0 (Receptors, KIR3DL1)
SB  - IM
EIN - J Exp Med. 2006 Apr 17;203(4):1131
MH  - Female
MH  - Gene Expression Regulation/genetics/immunology
MH  - Genetics, Population/methods
MH  - HLA-C Antigens/*genetics/immunology
MH  - Haplotypes/genetics/immunology
MH  - Humans
MH  - Japan
MH  - Killer Cells, Natural/*immunology
MH  - Lymphocyte Activation/*genetics/immunology
MH  - Male
MH  - Polymorphism, Genetic/*genetics/immunology
MH  - Receptors, Immunologic/*genetics/immunology
MH  - Receptors, KIR
MH  - Receptors, KIR2DL4
MH  - Receptors, KIR3DL1
MH  - Sex Factors
PMC - PMC2118260
EDAT- 2006/03/15 09:00
MHDA- 2006/05/04 09:00
PMCR- 2006/09/20
CRDT- 2006/03/15 09:00
PHST- 2006/03/15 09:00 [pubmed]
PHST- 2006/05/04 09:00 [medline]
PHST- 2006/03/15 09:00 [entrez]
PHST- 2006/09/20 00:00 [pmc-release]
AID - jem.20051884 [pii]
AID - 20051884 [pii]
AID - 10.1084/jem.20051884 [doi]
PST - ppublish
SO  - J Exp Med. 2006 Mar 20;203(3):633-45. doi: 10.1084/jem.20051884. Epub 2006 Mar 
      13.