PMID- 21299523
OWN - NLM
STAT- MEDLINE
DCOM- 20110610
LR  - 20231213
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 77
IP  - 3
DP  - 2011 Mar
TI  - Linkage disequilibrium between HLA-G*0104 and HLA-E*0103 alleles in Tswa Pygmies.
PG  - 193-200
LID - 10.1111/j.1399-0039.2010.01599.x [doi]
AB  - Nonclassical human leukocyte antigen (HLA)-G and -E loci are separated by 
      approximately 660 kb on the short arm of chromosome 6. Interestingly, some 
      functional and expression characteristics are relatively identical or associated 
      for both molecules. For example, expression of HLA-E on the cell surface has been 
      linked to preferential binding of nonameric leader peptides derived from the 
      signal sequence of HLA-G. It has been suggested that these two molecules act 
      synergistically in modulating susceptibility to infectious or chronic 
      inflammatory diseases. A possible explanation for these observations is that 
      HLA-E and HLA-G are evolving under analogous selective pressures and have 
      functions that place them under selective regimes differing from classical HLA 
      genes. The purpose of this study was to investigate the consistency of this 
      hypothesis based on the characterization of the molecular polymorphism of these 
      two genes and their linkage disequilibrium (LD) in three populations, i.e. 
      Southeastern French (n = 57), Teke Congolese (n = 84) and Tswa Pygmies (n = 74). 
      Allelic frequencies observed for HLA-G and HLA-E and for 14-bp ins/del 
      polymorphism in the three populations were similar to those observed in the 
      literature for populations from corresponding geographic areas. Only one of the 
      recently described HLA-G polymorphisms (HLA-G*01:07-01:16) was found, i.e. 
      HLA-G*01:15 in one individual from Congo. We showed that two haplotypes in Tswa 
      Pygmies, i.e. HLA-G*01:04-E*01:03:01 and G*01:04-E*01:01, exhibited highly 
      significant positive and negative D' values respectively. Although these LD could 
      have functional implications, it is more likely because of the genetic drift as 
      the two other populations did not display any significant LD.
CI  - (c) 2011 John Wiley & Sons A/S.
FAU - Di Cristofaro, J
AU  - Di Cristofaro J
AD  - UMR 6578 (Anthropobiologie Bioculturelle), Universite de la Mediterranee, CNRS, 
      EFS, Marseille, France.
FAU - Buhler, S
AU  - Buhler S
FAU - Frassati, C
AU  - Frassati C
FAU - Basire, A
AU  - Basire A
FAU - Galicher, V
AU  - Galicher V
FAU - Baier, C
AU  - Baier C
FAU - Essautier, A
AU  - Essautier A
FAU - Regnier, A
AU  - Regnier A
FAU - Granier, T
AU  - Granier T
FAU - Lepfoundzou, A D
AU  - Lepfoundzou AD
FAU - Chiaroni, J
AU  - Chiaroni J
FAU - Picard, C
AU  - Picard C
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
EIN - Tissue Antigens. 2011 Apr;77(4):364. Julie, D C [corrected to Di Cristofaro, J]
MH  - Alleles
MH  - Black People/ethnology/*genetics
MH  - Congo/ethnology
MH  - Dwarfism/*ethnology/*genetics
MH  - France
MH  - Gene Frequency
MH  - HLA Antigens/*genetics
MH  - HLA-G Antigens
MH  - Histocompatibility Antigens Class I/*genetics
MH  - Humans
MH  - INDEL Mutation
MH  - Linkage Disequilibrium
MH  - Polymorphism, Single Nucleotide
MH  - Population Groups/genetics
MH  - White People/genetics
MH  - HLA-E Antigens
EDAT- 2011/02/09 06:00
MHDA- 2011/06/11 06:00
CRDT- 2011/02/09 06:00
PHST- 2011/02/09 06:00 [entrez]
PHST- 2011/02/09 06:00 [pubmed]
PHST- 2011/06/11 06:00 [medline]
AID - 10.1111/j.1399-0039.2010.01599.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2011 Mar;77(3):193-200. doi: 10.1111/j.1399-0039.2010.01599.x.