PMID- 12799197
OWN - NLM
STAT- MEDLINE
DCOM- 20040310
LR  - 20111117
IS  - 0966-3274 (Print)
IS  - 0966-3274 (Linking)
VI  - 11
IP  - 2
DP  - 2003 Apr-Jun
TI  - Co-effect of HLA-G1 and glycosyltransferases in reducing NK cell-mediated pig 
      endothelial cell lysis.
PG  - 147-53
AB  - Natural killer (NK) cells play an important role in xenograft rejection. The aim 
      of this study was to evaluate the co-effect of human leukocyte antigen (HLA)-G1 
      expression and the remodeling of glycoantigens such as the alpha-Gal epitope, 
      Galalpha1,3Galbeta1,4GlcNAc-R, by the introduction of glycosyltransferase genes 
      related to NK cell-mediated direct cytotoxicity. Human peripheral blood 
      mononuclear cells or an NK-like cell line, YT cells, was used as an effector and 
      pig endothelial cells (PEC) as the target. A PEC transfectant with HLA-G1 was 
      first prepared by the transfection of HLA-G1 and human beta2 microglobulin. 
      Several new transfectants were then established by the transfection of 
      glycosyltransferase to the HLA-G1 transfectant. The effect of HLA-G1 on NK 
      cell-mediated PEC lysis was lower than that by the glycosyltransferases. 
      Therefore, in the case of the co-transfectants except for 
      HLA-G1+alpha2,6sialyltransferase, such as 
      HLA-G1+N-acetylglucosaminyltransferase-III and HLA-G1+alpha1,2fucosyltransferase, 
      the effect of HLA-G1 expression on NK-mediated killing appeared to be accounted 
      for by the transfected glycosyltransferase activities and the reduced alpha-Gal 
      expression on the cell surface. However, these transfectants showed significant 
      reductions in direct NK cell-mediated cytotoxicity, compared with the single 
      HLA-G1 transfectant. The results herein suggest that a combination of HLA-G1 and 
      glycosyltransferases has considerable potential for the downregulation of NK 
      cell-mediated cytolysis.
FAU - Miyagawa, Shuji
AU  - Miyagawa S
AD  - Division of Organ Transplantation, Department of Regenerative Medicine, Osaka 
      University Graduate School of Medicine, 2-2 Yamadaoka, Suita, 565-0871, Osaka, 
      Japan. miyagawa@orgtrp.med.osaka-u.ac.jp
FAU - Nakai, Rie
AU  - Nakai R
FAU - Matsunami, Katsuyoshi
AU  - Matsunami K
FAU - Kusama, Tamiko
AU  - Kusama T
FAU - Shirakura, Ryota
AU  - Shirakura R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Transpl Immunol
JT  - Transplant immunology
JID - 9309923
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - EC 2.4.- (Glycosyltransferases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - *Cytotoxicity, Immunologic
MH  - Down-Regulation
MH  - Endothelial Cells/immunology/*pathology
MH  - Flow Cytometry
MH  - Glycosyltransferases/genetics/*immunology
MH  - HLA Antigens/genetics/*immunology
MH  - HLA-G Antigens
MH  - Histocompatibility Antigens Class I/genetics/*immunology
MH  - Humans
MH  - Killer Cells, Natural/*immunology
MH  - Swine
MH  - Transfection
EDAT- 2003/06/12 05:00
MHDA- 2004/03/11 05:00
CRDT- 2003/06/12 05:00
PHST- 2003/06/12 05:00 [pubmed]
PHST- 2004/03/11 05:00 [medline]
PHST- 2003/06/12 05:00 [entrez]
AID - S0966-3274(02)00151-X [pii]
AID - 10.1016/S0966-3274(02)00151-X [doi]
PST - ppublish
SO  - Transpl Immunol. 2003 Apr-Jun;11(2):147-53. doi: 10.1016/S0966-3274(02)00151-X.