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KIR3DL1+HLA‐B Bw4 Ile80 and KIR2DS1+HLA‐C2 combinations are both associated with ankylosing spondylitis in the Iranian population
Author(s) -
Tajik N.,
Shahsavar F.,
Poormoghim H.,
Radjabzadeh M. F.,
Mousavi T.,
Jalali A.
Publication year - 2011
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.2011.01024.x
Subject(s) - human leukocyte antigen , genotype , ankylosing spondylitis , genotyping , immunology , pathogenesis , population , hla b , receptor , biology , antigen , genetics , medicine , gene , environmental health
Summary Contribution of killer cell immunoglobulin‐like receptors (KIR) and their human leucocyte antigen (HLA) class I ligands in the pathogenesis of autoimmune diseases has been shown in several studies. In this study, the possible association of KIR genes, their known HLA ligands and compound KIR/HLA genotypes with ankylosing spondylitis (AS) was assessed. Combined KIR/HLA ligand genotyping was performed by a polymerase chain reaction–sequence‐specific primers assay in 35 Iranian patients with AS, and genotypes were compared to those in 200 healthy individuals. The frequencies of telomeric cluster genes KIR2DL5A , KIR2DS1 and KIR3DS1 were significantly increased in AS patient group ( P c  = 0.0082, P c  = 0.0195 and P c  = 0.0328, respectively). Conversely, HLA‐Bw4 ligand (the presence of one or more ‐B Bw4 Ile80 , ‐B Bw4 Thr80 and ‐A Bw4 epitopes) ( P c  = 0.0004) and HLA‐B Bw4 Ile80 ( P c  = 0.053) were less frequent in these patients. Meanwhile, compound KIR/HLA genotype analyses revealed lower frequency of KIR3DL1 + HLA‐B Bw4 Ile80 ( P c  = 0.0343) and higher frequency of KIR2DS1+HLA‐C2 ( P c  = 0.0308) combinations in patients with AS than in controls. In addition, the genotypes iKIR+HLA>aKIR+HLA ( P c  = 0.0308) and iKIR+HLA>aKIR ( P c  = 0.0258) were statistically less common, and genotypes iKIR+HLA=aKIR+HLA ( P c  = 0.0081) and iKIR+HLA

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