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Arthritis Res Ther. 2006; 8(4): R101.
Published online Jun 28, 2006. doi:  10.1186/ar1988
PMCID: PMC1779409
Contribution of KIR3DL1/3DS1 to ankylosing spondylitis in human leukocyte antigen-B27 Caucasian populations
Carlos Lopez-Larrea,corresponding author1 Miguel Angel Blanco-Gelaz,1 Juan Carlos Torre-Alonso,2 Jacome Bruges Armas,3 Beatriz Suarez-Alvarez,1 Laura Pruneda,1 Ana Rita Couto,3 Segundo Gonzalez,4 Antonio Lopez-Vázquez,1 and Jesus Martinez-Borra1
1Histocompatibility and Transplantation Unit, Hospital Universtario Central de Asturias, Celestino Villamil s/n. 33006 Oviedo, Asturias, Spain
2Rheumatology Unit, Hospital Monte Naranco, Avda Dres Fernandez Vega 107. 33012 Oviedo, Asturias, Spain
3Immunogenetic Service, Hospital de Santo Espirito de Angra do Heroismo, Vinha Brava. 9700 Angra do Heroismo, Azores, Portugal
4Functional Biology Department, University of Oviedo, Avda Julian Claveria s/n. 33006 Oviedo, Asturias, Spain
corresponding authorCorresponding author.
Carlos Lopez-Larrea: inmuno/at/hca.es; Jesus Martinez-Borra: mtnezborra/at/hotmail.com
Received March 10, 2006; Revisions requested March 23, 2006; Revised April 5, 2006; Accepted June 5, 2006.
Abstract
Killer cell immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) loci are both highly polymorphic, and some HLA class I molecules bind and trigger cell-surface receptors specified by KIR genes. We examined whether the combination of KIR3DS1/3DL1 genes in concert with HLA-B27 genotypes is associated with susceptibility to ankylosing spondylitis (AS). Two HLA-B27-positive Caucasian populations were selected, one from Spain (71 patients and 105 controls) and another from the Azores (Portugal) (55 patients and 75 controls). All were typed for HLA-B and KIR (3DS1 and 3DL1) genes. Our results show that in addition to B27, the allele 3DS1 is associated with AS compared with B27 controls (p < 0.0001 and p < 0.003 in the Spanish population and Azoreans, respectively). We also observed that the association of KIR3DS1 to AS was found in combination with HLA-B alleles carrying Bw4-I80 in trans position in the Spanish population (30.9% in AS versus 15.2% in B27 controls, p = 0.02, odds ratio (OR) = 2.49) and in Azoreans (27.2% in AS versus 8.7% in B27 controls, p = 0.01, OR = 4.4 in Azoreans). On the other hand, 3DL1 was decreased in patients compared with B27 controls (p < 0.0001 in the Spanish population and p < 0.003 in Azoreans). The presence of this allele in combination with Bw4-I80 had a protective effect against the development of AS in the Spanish population (19.7% in AS, 35.2% in B27 controls; p = 0.03, OR = 0.45). The presence of KIR3DS1 or KIR3DL1 in combination with HLA-B*27s/HLA-B Bw4-I80 genotypes may modulate the development of AS. The susceptibility to AS could be determined by the overall balance of activating and inhibitory composite KIR-HLA genotypes.
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