Clinical Dermatology Research JournalISSN: 2576-1439

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Interferon –γ Gene Polymorphism as a Biochemical Marker for Atopic dermatitis in Saudis

Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory skin disease characterized by severe itching and recurrent, relapsing eczema-like skin lesions, affecting up to 15% of children in industrialized countries. AD is a complex multifactorial disease, and its exact etiology and pathogenesis have not been fully elucidated. The aim of this study was to investigate the impact of gene polymorphisms of T helper cell subtype Th1 cytokine, interferon-gamma (IFN-γ) on AD susceptibility in a Saudi cohort.  Hundred four unrelated patients with AD and 195 healthy controls were genotyped for IFN-γ (874A/T) polymorphism. Genomic DNA was separated from the fringe blood of AD patients and controls utilizing the QIAampR DNA little unit. IFN-γ quality was enhanced utilizing intensification headstrong transformation frameworks (ARMS)- PCR philosophy to identify polymorphisms at position 874 of IFN-γ. The frequency of genotype AT of IFN-γ (874A/T) was significantly higher while genotype AA was lower in AD patients as compared to controls (P <0.001). The frequency of T containing genotypes (AT+TT) was also higher in AD patients as compared to that in controls (P = 0.001). The frequencies of allele T and A were statistically different in patients and controls (P = 0.04). These results indicated that genotype AT of IFN-γ (874A/T) polymorphism is associated with AD risk and genotype AA is protective to AD. It is concluded that IFN-γ (874A/T) polymorphism is associated with the susceptibility of AD, however further studies with a large sample size involving different ethnic populations should be conducted to strengthen these results.

Special Features

Full Text

View

Track Your Manuscript

Media Partners

GET THE APP