Association of KIR genotype with susceptibility to HLA-B27-positive ankylosing spondylitis

ObjectiveRecent studies have explored the role of killer cell immunoglobulin-like receptors (KIRs) in chronic autoimmune diseases. The purpose of this study was to demonstrate whether KIR genes contribute to the pathogenesis of ankylosing spondylitis (AS) in Chinese populations.MethodsSixteen KIR genes were genotyped from 60 unrelated patients with AS and 60 HLA-B27-positive matched healthy controls by PCR-SSP. The frequencies of the KIR alleles and genotypes in the AS and control groups were assessed by the χ2 test.ResultsOur results showed that the frequency of the activator receptor KIR3DS1 gene in the AS group was significantly increased compared to the controls (χ2 = 5.263, P = 0.006, OR = 3.059, 95 % CI = 1.357–6.896). Moreover, the frequency of the KIR3DL1/3DS1 genotype was greater in the AS group than in the control group (P = 0.039, OR = 3.059, 95 % CI = 1.357–6.896). In contrast, the frequency of the no KIR3DL1/no 3DS1 genotype was lower in patients with AS compared with the controls (P = 0.032, OR = 0.110, 95 % CI = 0.013–0.911).ConclusionKIR3DS1, in addition to HLA-B27, may play an important independent role in the pathogenesis of AS in the Chinese population.

[1]  O. Britanova,et al.  Contribution of functional KIR3DL1 to ankylosing spondylitis , 2010, Cellular and Molecular Immunology.

[2]  M. Brown Progress in spondylarthritis. Progress in studies of the genetics of ankylosing spondylitis , 2009, Arthritis research & therapy.

[3]  D Middleton,et al.  Analysis of killer immunoglobulin-like receptor genes in ankylosing spondylitis , 2008, Annals of the rheumatic diseases.

[4]  Y. Jiao,et al.  Polymorphisms of KIRs Gene and HLA-C Alleles in Patients with Ankylosing Spondylitis: Possible Association with Susceptibility to the Disease , 2008, Journal of Clinical Immunology.

[5]  Edgar Erdfelder,et al.  G*Power 3: A flexible statistical power analysis program for the social, behavioral, and biomedical sciences , 2007, Behavior research methods.

[6]  B. Suarez-Alvarez,et al.  Contribution of KIR3DL1/3DS1 to ankylosing spondylitis in human leukocyte antigen-B27 Caucasian populations , 2006, Arthritis research & therapy.

[7]  Jeff P. Reeve,et al.  Association of the IL1 gene cluster with susceptibility to ankylosing spondylitis: an analysis of three Canadian populations. , 2006, Arthritis and rheumatism.

[8]  L. Bradbury,et al.  Concordance of disease severity among family members with ankylosing spondylitis? , 2004, The Journal of rheumatology.

[9]  M. Brown,et al.  Genetic susceptibility to ankylosing spondylitis. , 2004, Current molecular medicine.

[10]  M. Snyder,et al.  The double life of NK receptors: stimulation or co-stimulation? , 2004, Trends in immunology.

[11]  A. Toubert,et al.  Functional modulation of expanded CD8+ synovial fluid T cells by NK cell receptor expression in HLA-B27-associated reactive arthritis. , 2002, International immunology.

[12]  Michael J. Wilson,et al.  Cutting Edge: Leukocyte Receptor Complex-Encoded Immunomodulatory Receptors Show Differing Specificity for Alternative HLA-B27 Structures1 , 2001, The Journal of Immunology.

[13]  D. Weeks,et al.  Whole-genome screening in ankylosing spondylitis: evidence of non-MHC genetic-susceptibility loci. , 2001, American journal of human genetics.

[14]  D. Schaid,et al.  Expansion of unusual CD4+ T cells in severe rheumatoid arthritis. , 1997, Arthritis and rheumatism.

[15]  A. Cats,et al.  Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. , 1984, Arthritis and rheumatism.