Background: Psoriasis is a chronic, non infectious, relapsing inflammatory skin disease caused by genetic, immunological and other factors in the environment, affecting 2–5% of the world’s population . Granulysin is an anti-microbial peptide that contributes to local amplification of inflammation. The activation and maintenance of the T helper 17 pathway is the essential role of of IL23 in the pathogenesis of psoriasis. Objectives: Evaluation of the relation of granulysin (GNLY) gene single nucleotide polymorphism to psoriasis pathogenesis, measurement of interleukin23 (IL23) level in sera of cases of psoriasis and its relation to disease severity. Methodology: our study was done on 50 subjects divided into 2 groups:30 psoriasis patients, selected from Outpatients Clinics of Dermatology, Venerology and Andrology Department of Benha University Hospitals, and 20 apparent healthy control subjects of matched sex and age. Four ml venous blood samples were collected from psoriasis patients and control subjects to genotype GNLY rs7908 (C/G) and GNLY rs10180391(C/T) polymorphisms by Polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP)-based analysis and detection of interleukin (IL23) level using ELISA. Results: GNLY rs7908 CC genotype was significantly lower in psoriasis patients (6.7%) than in the control group (30%). The difference between patients and controls for GNLY rs10180391 allele frequencies was not statistically significant. IL23 level increased significantly with increased severity of psoriasis. Conclusion: GNLY rs 7908 gene polymorphism had a significant relation with severity of psoriasis. IL23 level was directly proportional to the severity of psoriasis. |
