A weak association of HLA-B*2702 with Behcet's disease

Gul A., Uyar F. A., Inanc M., Ocal L., Barrett J., Aral O., ...Daha Fazla

GENES AND IMMUNITY, cilt.3, sa.6, ss.368-372, 2002 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 3 Sayı: 6
  • Basım Tarihi: 2002
  • Doi Numarası: 10.1038/sj.gene.6363863
  • Dergi Adı: GENES AND IMMUNITY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.368-372
  • Anahtar Kelimeler: Behcet's disease, HLA-B*2702, HLA-B51, immunoglobulin-like killer inhibitory receptor (KIR), NK cell, relative predispositional effects, allelic association, NATURAL-KILLER-CELLS, HLA-B, T-CELLS, INHIBITORY RECEPTOR, ALLELES, HLA-B51, POLYMORPHISM, RECOGNITION, RESPONSES, GAMMA
  • İstanbul Üniversitesi Adresli: Evet

Özet

This study aimed to analyse the association of HLA-B alleles other than -B51 with Behcet's disease (BD), We also investigated the frequency of HLA-B alleles sharing the same natural killer cell immunoglobulin-like receptor (KIR) binding sequence with HLA-B51. Broad-genotyping of HLA-B locus by PCR-SSOP in 174 Turkish BD patients and 191 healthy controls confirmed the strong association of B*51 with BD (60.9% in BD patients, 24.6% in healthy controls, OR=4.78). No other HLA-B allele was identified showing an association with BD after adjusting for multiple testing or by using relative predispositional effects (RPE) analysis after the deletion of B*51. HLA-B alleles reacting with the sequence specific oligonucleotide probe 23, which corresponds to the KIR binding site of B*51, were found to be positive in 127 BD patients (73%) and 90 controls (47%) (OR=3.03, 95% Cl 2-4.7). The repeated RPE analysis after separating HLA-B alleles carrying B51-KIR binding sequence as distinct alleles within a broad-type allele group revealed B*2702 allele as the only allele showing an association with BD after the deletion of B*51. Selective Increase of B*2702, the only B*27 allele carrying the same KIR binding sequence with B*51, warrants investigation of the possibility of interaction of HLA molecules with KIRs on NK or other T cells in the pathogenesis of BD.