PMID- 15546338
OWN - NLM
STAT- MEDLINE
DCOM- 20050419
LR  - 20220331
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 64
IP  - 6
DP  - 2004 Dec
TI  - TNF-alpha and TGF-beta1 gene polymorphisms and renal allograft rejection in 
      Koreans.
PG  - 660-6
AB  - This study was performed in order to evaluate the association of tumour necrosis 
      factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) gene 
      polymorphisms with renal allograft rejection in Koreans. Five TNF-alpha 
      (-1031T/C, -863C/A, -857C/T, -308G/A and -238G/A) and two TGF-beta1 (codon 10 T/C 
      and codon 25 G/C) single-nucleotide polymorphism (SNP) sites were studied by 
      using polymerase chain reaction (PCR) single-strand conformation polymorphism and 
      PCR restriction fragment length polymorphism methods in 100 controls and 164 
      patients. The patients underwent renal transplantation, having one or more Human 
      leukocyte antigen (HLA)-A, HLA-B and HLA-DR antigens mismatched with their 
      donors. For the TGF-beta1 gene, we also studied the polymorphism of donors. The 
      allele frequencies of each SNP site in controls were not different from those of 
      patients. The frequency of TNF-alpha high-producer genotype, -308GA, and 
      TGF-beta1 lower (intermediate)-producer genotype, codon 10 CC and codon 25 GG, 
      were significantly higher in patients with recurrent acute rejection episodes 
      (REs), compared to those in patients with no or one RE. The highest risk group 
      for developing recurrent REs showed the combination of TNF-alpha high- and 
      TGF-beta1 lower-producer genotypes. Analysis of chronic renal allograft 
      dysfunction (CRAD) revealed that TGF-beta1 high-producer genotype of donors, 
      codon 10 TT/TC and codon 25 GG, is associated with CRAD especially in patients 
      with recurrent REs. The highest risk group for developing CRAD showed the 
      combination of recipient's TNF-alpha high- and donor's TGF-beta1 high-producer 
      genotypes. These results would be useful for predicting high-risk group for acute 
      rejection or CRAD in renal transplantation.
FAU - Park, J-Y
AU  - Park JY
AD  - Department of Laboratory Medicine, Seoul National University College of Medicine, 
      Seoul, South Korea.
FAU - Park, M H
AU  - Park MH
FAU - Park, H
AU  - Park H
FAU - Ha, J
AU  - Ha J
FAU - Kim, S J
AU  - Kim SJ
FAU - Ahn, C
AU  - Ahn C
LA  - eng
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 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Chronic Disease
MH  - Gene Frequency
MH  - Genotype
MH  - Graft Rejection/*genetics
MH  - HLA Antigens/metabolism
MH  - Humans
MH  - Kidney/*metabolism
MH  - Kidney Diseases/*etiology
MH  - Kidney Transplantation/*adverse effects
MH  - Korea
MH  - Polymerase Chain Reaction
MH  - *Polymorphism, Single Nucleotide
MH  - Polymorphism, Single-Stranded Conformational
MH  - Transforming Growth Factor beta/*genetics/metabolism
MH  - Transforming Growth Factor beta1
MH  - Transplantation, Homologous
MH  - Tumor Necrosis Factor-alpha/*genetics/metabolism
EDAT- 2004/11/18 09:00
MHDA- 2005/04/20 09:00
CRDT- 2004/11/18 09:00
PHST- 2004/11/18 09:00 [pubmed]
PHST- 2005/04/20 09:00 [medline]
PHST- 2004/11/18 09:00 [entrez]
AID - TAN330 [pii]
AID - 10.1111/j.1399-0039.2004.00330.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2004 Dec;64(6):660-6. doi: 10.1111/j.1399-0039.2004.00330.x.