PMID- 12559621
OWN - NLM
STAT- MEDLINE
DCOM- 20030926
LR  - 20221207
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 64
IP  - 2
DP  - 2003 Feb
TI  - Assessment of killer cell immunoglobulinlike receptor expression and 
      corresponding HLA class I phenotypes demonstrates heterogenous KIR expression 
      independent of anticipated HLA class I ligands.
PG  - 183-93
AB  - Natural killer (NK) cell-mediated cytolysis is stimulated and downregulated 
      through the interaction of distinct human leukocyte antigen (HLA) class I 
      molecules on target cells with specific killer cell immunoglobulinlike receptors 
      (KIRs) on NK cells. Killer cell immunoglobulinlike receptors are highly 
      polymorphic and are clonally distributed on NK cell populations within 
      individuals. However, the regulation of KIR expression by individual HLA class I 
      phenotypes is not well understood. To examine a potential influence of the HLA 
      class I phenotype on KIR expression patterns we studied the KIR expression in 
      individuals that were subgrouped according to the major HLA-C encoded 
      KIR-epitopes (group C1 versus C2). In these individuals, NK cells were analyzed 
      for KIR expression using flow cytometry and RNA-based expression analysis. Our 
      results demonstrate that KIR genes are transmitted very heterogeneously with two 
      main patterns of KIR genotypes as previously described; group A and group B (with 
      21 different genotypes). There are distinct populations exhibiting different 
      densities of CD158a and/or CD158b positive NK cells that coexist in all 
      individuals. A clear correlation between KIR expression and the currently known 
      HLA class I ligands was not observed. In conclusion, the surface expression of 
      KIRs in individuals with different HLA class I genotypes indicates that other 
      non-HLA class I encoded factors contribute to the shaping of the KIR repertoire.
FAU - Becker, Sven
AU  - Becker S
AD  - Institute of Transfusion Medicine and Immunohematology, RCBDS, Frankfurt, 
      Germany.
FAU - Tonn, Torsten
AU  - Tonn T
FAU - Fussel, Tobias
AU  - Fussel T
FAU - Uhrberg, Markus
AU  - Uhrberg M
FAU - Bogdanow, Manuela
AU  - Bogdanow M
FAU - Seifried, Erhard
AU  - Seifried E
FAU - Seidl, Christian
AU  - Seidl C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Ligands)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, KIR)
RN  - 0 (Receptors, KIR2DL1)
RN  - 0 (Receptors, KIR2DL3)
SB  - IM
MH  - Blood Donors
MH  - Chromosome Segregation
MH  - Chromosomes, Human, Pair 19/genetics
MH  - Chromosomes, Human, Pair 6/genetics
MH  - Clone Cells/metabolism
MH  - *Gene Expression Regulation
MH  - Gene Frequency
MH  - Genotype
MH  - Germany
MH  - Haplotypes/genetics
MH  - Histocompatibility Antigens Class I/*genetics
MH  - Histocompatibility Testing
MH  - Humans
MH  - Killer Cells, Natural/classification/metabolism
MH  - Ligands
MH  - Linkage Disequilibrium
MH  - Phenotype
MH  - Receptors, Immunologic/biosynthesis/*genetics
MH  - Receptors, KIR
MH  - Receptors, KIR2DL1
MH  - Receptors, KIR2DL3
MH  - White People/genetics
EDAT- 2003/02/01 04:00
MHDA- 2003/09/27 05:00
CRDT- 2003/02/01 04:00
PHST- 2003/02/01 04:00 [pubmed]
PHST- 2003/09/27 05:00 [medline]
PHST- 2003/02/01 04:00 [entrez]
AID - S0198885902008029 [pii]
AID - 10.1016/s0198-8859(02)00802-9 [doi]
PST - ppublish
SO  - Hum Immunol. 2003 Feb;64(2):183-93. doi: 10.1016/s0198-8859(02)00802-9.