Genetic variants in IFIH1 play opposite roles in the pathogenesis of psoriasis and chronic periodontitis
Yazarlar (9)
Fudan University, Çin
Fudan University, Çin
Chinese Academy of Sciences, Çin
Prof. Dr. Mustafa KAN
Chinese Academy of Sciences, Çin
Chinese Academy of Sciences, Çin
Shanghai Jiao Tong University, Çin
Chinese Academy of Sciences, Çin
Fudan University, Çin
Fudan University, Çin
| Makale Türü | Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale) | ||
| Dergi Adı | INTERNATIONAL JOURNAL OF IMMUNOGENETICS | ||
| Dergi ISSN | 1744-3121 Wos Dergi Scopus Dergi | ||
| Makale Dili | İngilizce | Basım Tarihi | 04-2012 |
| Cilt / Sayı / Sayfa | 39 / 2 / 137–143 | DOI | 10.1111/j.1744-313X.2011.01068.x |
| Özet |
| The IFIH1 gene is a key factor connecting environmental and genetic factors in the pathogenesis of immune-related diseases. We aimed to investigate whether it has effects on psoriasis, chronic periodontitis and skin test-positive penicillin allergy and to confirm whether these diseases have shared molecular mechanisms originating from shared genetics. Two common variants in IFIH1 were genotyped in 561 patients with psoriasis, 421 patients with chronic periodontitis, 175 patients with skin test-positive penicillin allergy and 1100 shared controls. Then, casecontrol study was used to analyse the association between IFIH1 and the three diseases. The allele distributions of rs1990760 and rs3747517 in the Chinese population are much different from the European population. The A allele of rs1990760 (OR = 1.30, P = 5.4 x 10-3) and A-G (rs1990760/rs3747517) haplotype (OR = 1.31, P = 3.8 x 10-3) were highly associated with the risk of psoriasis. However, the A allele of rs1990760 (OR = 0.73, P = 7.8 x 10-3) and A-G haplotype (OR = 0.71, P = 4.5 x 10-3) were identified as protective factors for chronic periodontitis. IFIH1 affects several immune-related diseases, including psoriasis and chronic periodontitis, and provides a molecular link between genetic susceptibility, viral infections and immune-related diseases. Moreover, we also confirm the hypothesis that shared molecular mechanisms from common genetic variants contribute to a spectrum of immune-related diseases. |
| Anahtar Kelimeler |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları | |
| WoS | 16 |