Abstract:
BACKGROUND:Association studies of genes encoding cytokines that play an important role in inflammatory response represent one approach to finding type 1 diabetes (T1D) disease genes. The aim of this study was to investigate the association of single nucleotide polymorphisms (SNPs) within cytokine genes with T1D in a cohort of Saudi subjects. METHODS:A total of 300 well-characterized type 1 diabetic patients and 300 T1D-free control subjects were enrolled in this investigation. Cytokine SNPs were genotyped by using Polymerase chain reaction (PCR) with sequence-specific primers. RESULTS:Our data revealed that IFN-γ +874T allele carriers [odds ratio (OR) = 1.87, p < 0.001] and TT homozygotes (OR = 1.28, p < 0.001) were significantly more susceptible to developing T1D than the A allele carriers. In addition, TNF-α -308A allele carriers (OR = 1.73, p < 0.001) and AA homozygotes (OR = 1.74, p < 0.001) were also overrepresented among the diabetics than G allele carriers. IL-4 -590C/T TT homozygotes (OR = 2.23, p < 0.001) were significantly more susceptible to develop T1D than CC genotypes, whereas CT heterozygotes were not significantly associated (OR = 1.43, p = 0.78) with T1D. Furthermore, IL-4 T allele was statistically associated with T1D patients compared to control group (OR = 2.24, p < 0.001). Similarly, IL-1β -511C/T TT homozygotes (OR = 1.85, p = 0.012) and the T allele (OR = 1.85, p < 0.001) were significantly more susceptible to T1D than CC genotypes, whereas TC heterozygotes (OR = 1.04, p = 0.86) were not significantly associated with T1D. CONCLUSION:Our data concluded that IFN-γ +874T allele, TNF-α -308A allele, IL-1β -511T allele, and IL-4 -590T allele could be considered risk factors for T1D development in Saudi subjects.
journal_name
Immunol Investjournal_title
Immunological investigationsauthors
Allam G,Nasr A,Talaat IM,Abuelsaad ASA,Bakheit AM,Nemenqani D,Alsulaimani AAdoi
10.1080/08820139.2017.1416398subject
Has Abstractpub_date
2018-04-01 00:00:00pages
229-240issue
3eissn
0882-0139issn
1532-4311journal_volume
47pub_type
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