PMID- 20818412
OWN - NLM
STAT- MEDLINE
DCOM- 20110302
LR  - 20221207
IS  - 2042-0226 (Electronic)
IS  - 1672-7681 (Print)
IS  - 1672-7681 (Linking)
VI  - 7
IP  - 6
DP  - 2010 Nov
TI  - Contribution of functional KIR3DL1 to ankylosing spondylitis.
PG  - 471-6
LID - 10.1038/cmi.2010.42 [doi]
AB  - Increasing evidence points to a role for killer immunoglobulin-like receptors 
      (KIRs) in the development of autoimmune diseases. In particular, a positive 
      association of KIR3DS1 (activating receptor) and a negative association of 
      KIR3DL1 (inhibitory receptor) alleles with ankylosing spondylitis (AS) have been 
      reported by several groups. However, none of the studies analyzed these 
      associations in the context of functionality of polymorphic KIR3DL1. To better 
      understand how the KIR3DL1/3DS1 genes determine susceptibility to AS, we analyzed 
      the frequencies of alleles and genotypes encoding functional (KIR3DL1*F) and 
      non-functional (KIR3DL1*004) receptors. We genotyped 83 AS patients and 107 human 
      leukocyte antigen (HLA)-B27-positive healthy controls from the Russian Caucasian 
      population using a two-stage sequence-specific primer PCR, which distinguishes 
      KIR3DS1, KIR3DL1*F and KIR3DL1*004 alleles. For the patients carrying two 
      functional KIR3DL1 alleles, those alleles were additionally genotyped to identify 
      KIR3DL1*005 and KIR3DL1*007 alleles, which are functional but are expressed at 
      low levels. KIR3DL1 was negatively associated with AS at the expense of KIR3DL1*F 
      but not of KIR3DL1*004. This finding indicates that the inhibitory KIR3DL1 
      receptor protects against the development of AS and is not simply a passive 
      counterpart of the segregating KIR3DS1 allele encoding the activating receptor. 
      However, analysis of genotype frequencies indicates that the presence of KIR3DS1 
      is a more important factor for AS susceptibility than the absence of KIR3DL1*F. 
      The activation of either natural killer (NK) or T cells via the KIR3DS1 receptor 
      can be one of the critical events in AS development, while the presence of the 
      functional KIR3DL1 receptor has a protective effect. Nevertheless, even 
      individuals with a genotype that carried two inhibitory KIR3DL1 alleles expressed 
      at high levels could develop AS.
FAU - Zvyagin, Ivan V
AU  - Zvyagin IV
AD  - Shemiakin-Ovchinnikov Institute of Bioorganic Chemistry, RAS, Moscow, Russia.
FAU - Mamedov, Ilgar Z
AU  - Mamedov IZ
FAU - Britanova, Olga V
AU  - Britanova OV
FAU - Staroverov, Dmitriy B
AU  - Staroverov DB
FAU - Nasonov, Evgeni L
AU  - Nasonov EL
FAU - Bochkova, Anna G
AU  - Bochkova AG
FAU - Chkalina, Anna V
AU  - Chkalina AV
FAU - Kotlobay, Alexei A
AU  - Kotlobay AA
FAU - Korostin, Dmitriy O
AU  - Korostin DO
FAU - Rebrikov, Denis V
AU  - Rebrikov DV
FAU - Lukyanov, Sergey
AU  - Lukyanov S
FAU - Lebedev, Yuri B
AU  - Lebedev YB
FAU - Chudakov, Dmitriy M
AU  - Chudakov DM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100906
PL  - China
TA  - Cell Mol Immunol
JT  - Cellular & molecular immunology
JID - 101242872
RN  - 0 (KIR3DL1 protein, human)
RN  - 0 (Receptors, KIR3DL1)
RN  - 0 (Receptors, KIR3DS1)
SB  - IM
CIN - Nat Rev Rheumatol. 2010 Nov;6(11):614. PMID: 21064239
MH  - Adult
MH  - Alleles
MH  - Case-Control Studies
MH  - Gene Frequency/genetics
MH  - Heterozygote
MH  - Humans
MH  - Middle Aged
MH  - Receptors, KIR3DL1/*genetics
MH  - Receptors, KIR3DS1/genetics
MH  - Russia
MH  - Spain
MH  - Spondylitis, Ankylosing/*genetics
MH  - White People/genetics
PMC - PMC4002958
EDAT- 2010/09/08 06:00
MHDA- 2011/03/03 06:00
PMCR- 2010/11/01
CRDT- 2010/09/07 06:00
PHST- 2010/09/07 06:00 [entrez]
PHST- 2010/09/08 06:00 [pubmed]
PHST- 2011/03/03 06:00 [medline]
PHST- 2010/11/01 00:00 [pmc-release]
AID - cmi201042 [pii]
AID - 10.1038/cmi.2010.42 [doi]
PST - ppublish
SO  - Cell Mol Immunol. 2010 Nov;7(6):471-6. doi: 10.1038/cmi.2010.42. Epub 2010 Sep 6.