PMID- 18297378
OWN - NLM
STAT- MEDLINE
DCOM- 20080923
LR  - 20220408
IS  - 0271-9142 (Print)
IS  - 0271-9142 (Linking)
VI  - 28
IP  - 4
DP  - 2008 Jul
TI  - Polymorphisms of KIRs gene and HLA-C alleles in patients with ankylosing 
      spondylitis: possible association with susceptibility to the disease.
PG  - 343-9
LID - 10.1007/s10875-008-9183-6 [doi]
AB  - INTRODUCTION: An emerging body of evidence is accumulating to suggest that killer 
      cell immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) class 
      I ligands contribute to the pathogenesis of diverse kinds of autoimmune diseases. 
      However, the functional effects of their polymorphism remain largely unknown to 
      date. Thus, the present study was undertaken to determine the association of the 
      polymorphisms KIRs gene and HLA-C alleles with the susceptibility to ankylosing 
      spondylitis (AS) by means of polymerase chain reaction/sequence-specific primers 
      for genotyping KIRs from genomic DNA of 119 patients with AS together with 128 
      healthy donors as a control group. RESULTS AND DISCUSSION: We found that the 
      frequencies of KIR3DS1 and KIR2DL5 were statistically significantly higher in the 
      patient group than those in the control group (P = 0.016 and P = 0.003, 
      respectively). Meanwhile, the percentage of patients, who were carrying two or 
      more of the activating KIRs, was higher than that of control group. With respect 
      to HLA-C alleles, individuals with AS showed an increased frequency of HLA-Cw02. 
      If HLA-C was divided into group 1 or group 2 based on whether there was an 
      asparagine or lysine present at position 80 of the alpha-chain, HLA-C group 2 was 
      more common in subjects with AS compared to control subjects. The genotype 
      2DS1+/HLA-C lys(80)+ was more common in subjects with AS. Moreover, the CD69 
      expression, a NK activation marker, remarkably increased in patient with AS. 
      CONCLUSION: In conclusions, this study suggests that KIR3DS1 may severe as AS 
      susceptive genes to trigger continuous injury of arthrosis. The imbalance of 
      activating and inhibitory KIR as well as HLA-C group 1 and group 2 may be the key 
      factor, which influences the pathogenesis of AS. Moreover, KIR2DS1 might 
      associate with the susceptibility of AS by influencing NK cell activity once 
      group 2 HLA-C ligands are present.
FAU - Jiao, Yu-Lian
AU  - Jiao YL
AD  - Central Laboratory, Shandong Provincial Hospital, Shandong University, Jinan 
      250021, People's Republic of China.
FAU - Ma, Chun-Yan
AU  - Ma CY
FAU - Wang, Lai-Cheng
AU  - Wang LC
FAU - Cui, Bin
AU  - Cui B
FAU - Zhang, Jie
AU  - Zhang J
FAU - You, Li
AU  - You L
FAU - Chen, Zi-Jiang
AU  - Chen ZJ
FAU - Li, Jian-Feng
AU  - Li JF
FAU - Zhao, Yue-Ran
AU  - Zhao YR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080223
PL  - Netherlands
TA  - J Clin Immunol
JT  - Journal of clinical immunology
JID - 8102137
RN  - 0 (HLA-C Antigens)
RN  - 0 (Receptors, KIR)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Child
MH  - Female
MH  - *Genetic Predisposition to Disease
MH  - HLA-C Antigens/*genetics
MH  - Humans
MH  - Killer Cells, Natural/immunology
MH  - Male
MH  - Middle Aged
MH  - *Polymorphism, Genetic
MH  - Receptors, KIR/*genetics
MH  - Spondylitis, Ankylosing/*genetics/immunology
EDAT- 2008/02/26 09:00
MHDA- 2008/09/24 09:00
CRDT- 2008/02/26 09:00
PHST- 2007/08/28 00:00 [received]
PHST- 2008/01/23 00:00 [accepted]
PHST- 2008/02/26 09:00 [pubmed]
PHST- 2008/09/24 09:00 [medline]
PHST- 2008/02/26 09:00 [entrez]
AID - 10.1007/s10875-008-9183-6 [doi]
PST - ppublish
SO  - J Clin Immunol. 2008 Jul;28(4):343-9. doi: 10.1007/s10875-008-9183-6. Epub 2008 
      Feb 23.