Toll-Like Receptors 2 and 4 Polymorphisms in Age-Related Macular Degeneration

Guven M., Batar B., Mutlu T., Bostanci M., Mete M., Aras C., ...Daha Fazla

CURRENT EYE RESEARCH, cilt.41, sa.6, ss.856-861, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 41 Sayı: 6
  • Basım Tarihi: 2016
  • Doi Numarası: 10.3109/02713683.2015.1067326
  • Dergi Adı: CURRENT EYE RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.856-861
  • Anahtar Kelimeler: Age-related macular degeneration, TLR polymorphism, POLYPOIDAL CHOROIDAL VASCULOPATHY, PATTERN-RECOGNITION RECEPTORS, RETINAL-PIGMENT EPITHELIUM, IMMUNE-SYSTEM, TLR4, NEOVASCULARIZATION, SUSCEPTIBILITY, HYALURONAN, ACTIVATION, EXPRESSION
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Purpose: Age-related macular degeneration (AMD) is a complex disorder with multifactorial etiology, caused by a combination of genetic and environmental factors. Innate immunity appears to play a key role in the pathogenesis of AMD. The purpose of this study was to determine whether common variation in the human toll-like receptors (TLRs) 2 and 4 alters the risk of AMD.Patients and methods: A total of 183 patients with AMD and 200 disease-free control subjects were enrolled. The genotyping of polymorphisms TLR2 (TLR2-Arg753Gln: rs5743708) and TLR4 (TLR4-Asp299Gly: rs4986790; TLR4-Thr399Ile: rs4986791) were done using real-time PCR.Results: TLR2 Arg753Gln genotype had approximately four times greater risk of AMD compared with TLR2 Arg753Arg genotype (OR=3.88; 95% CI: 1.76-8.75, p=0.001). TLR2 Arg753Gln genotype was significantly higher in the patients with dry-type AMD (16%) and wet-type AMD (18%) than in the control (5%) subjects (p=0.005 and p=0.0008, respectively). There were no significant differences in the distribution of TLR4-Asp299Gly and TLR4-Thr399Ile genotypes between AMD patients and controls (p>0.05).Conclusion: Our results suggest that TLR2 polymorphism may contribute to the pathogenesis of AMD.