Background: Psoriasis is a systemic inflammatory disorder that involves complex pathogenic interactions between the innate and adaptive immune systems. The most accepted mechanism in the etiopathogenesis of psoriasis is the induction of inflammation with keratinocyte hyperproliferation. Granulysin (GNLY) is a cytolytic antimicrobial peptide (AMP) that is secreted together with granzyme and perforin from the granules of human cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. It has been immunohistochemically proven that the expression of granulysin is increased in lesions of psoriasis. Objective: This study aimed to investigate the relationship between psoriasis disease and granulysin gene polymorphisms. Methods: GNLY rs7908 and rs10180391 polymorphisms were studied by PCR-RFLP in 100 psoriasis patients under treatment in the Dermatology Polyclinic of Bulent Ecevit University. In addition, 100 healthy individuals with similar age and sex distribution were used as a control group. Results: In the control group, GNLY rs7908 CC genotype was significantly higher than in psoriasis patients (P= 0.031; OR= 0.305; Cl= 0.305 (0.121 - 0.773). In our study, the genotype distributions in patients and control groups were GNLY rs7908 (SNP) GG (51%, 37%), GC (41%, 44%), CC (8%, 19%); GNLY rs10180391 (SNP) from the CC (41%, 44%), CT (42%, % 41), TT (17%, 15%). Study limitations: The study only included Turkish patients. Conclusion: Our findings showed that GNLY rs7908 CC genotype and C allele had a protective effect against psoriasis and decreased the disease severity (according to PASI score), whereas rs10180391 SNP did not show any effective role in psoriasis pathogenesis.

Background: Psoriasis is a common, chronic, inflammatory skin disease that involves changes taking place as a result of activation of the immune system. Suppressor of cytokine signaling proteins (SOCS) are intracellular proteins that act as endogenous inhibitors of proinflammatory pathways triggered by various cytokines. In this study, the relationship between psoriasis disease and SOCS gene polymorphisms is investigated in relation to the pathogenesis of psoriasis to clarify the psoriasis susceptibility profile. Methods:The SOCS3 rs4969169 and SOCS7 rs3748726 polymorphisms were detected using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The study was approved by the Clinical Research Ethics Committee of Bulent Ecevit University and performed in accordance with the ethical standards established in the 1964 Declaration of Helsinki and later amendments. All participants were informed of the parameters of the study, and they signed consent forms before being included.Statistical analysis was performed using the SPSS 18.0 (SPSS Inc.) package program. Results: For the SOCS3 rs4969169 genotype frequency, the CC/CT genotypes represented 67%/33% in the patient group and 73%/27% in the control group. For the SOCS7 rs3748726 genotype frequency, the TT/TC/CC genotypes made up 89%/9%/1% in the patient group and 91%/8%/1% in the control group. Conclusion:The polymorphisms of SOCS3 rs4969169 and SOCS7 rs3748726 were found to have no effective role in the pathogenesis of psoriasis. This is the first study to investigate this topic, and further studies with larger, more ethnically diverse samples are encouraged.

Psoriasis; sık rastlanan, deri ile birlikte eklemleri de etkileyebilen, kronik ve tekrarlayıcı bir hastalıktır. Psoriasisin etiyopatogenezi tam olarak açıklanamamış olsa da en çok desteklenen mekanizma, herhangi bir etkenle tetiklenen inflamasyondur. Son yıllarda tanımlanan toll benzeri reseptör (TLR) ailesinin oldukça geniş çeşitlilikteki patojenlere karşı konakçı bağışıklığında kritik bir rol oynadığı bilinmektedir. Çalışmamızda, bu hasta grubunda bazı TLR gen polimorfizmlerinin, psoriasis ile olan muhtemel ilişkilerinin ortaya konmasını amaçladık. Yöntemler: Psoriasis tanısı almış 100 hasta ile otoimmün veya inflamatuvar hastalığı olmadığı bilinen 173 hasta içeren sağlıklı kontrol grubu çalışmaya dahil edilmiş olup TLR2 geni Arg677Trp, Arg753Gln,-196-174 del ve TLR4 geni Asp299Gly, Thr399Ile polimorfizmleri polimeraz zincir reaksiyonu-restriksiyon parça uzunluk polimorfizmi yöntemi ile belirlenmiş, hasta ve kontrol grubu sözü edilen gen polimorfizmleri açısından karşılaştırılmıştır. Bulgular: Bu çalışma ile psoriasisin, TLR2 Arg753Gln polimorfizminde GA genotipi ve A aleli ile istatistiksel olarak anlamlı bir ilişkide olduğu saptanmıştır. Ayrıca-196-174 del gen polimorfizmi için hasta ve kontrol grubu karşılaştırıldığında, ins/del genotipine sahip olmanın koruyucu etki yaptığı belirlenmiştir. Sonuç: TLR2 genindeki varyant alellerin, psoriasisin moleküler etiyopatogenezinde önemli rolü olabileceğini düşünmekteyiz.

Aim: The aim of our study is to analyze the SIRT1 gene rs2273773, rs7895833 and rs7069102 polymorphisms and the association of SIRT1 gene and interacting genes with vitiligo disease by molecular and in silico methods. Material and Methods: The study group consisted of 78 vitiligo patients and 85 unrelated healthy controls. SIRT1 polymorphisms were determined using the Polymerase chain reaction confronting twopair primers (PCR-CTPP) method. In addition, other genes with which the SIRT1 gene interacts and gene ontology (GO) were determined using the GeneMANIA and GeneCodis 4 tools, respectively. Results: We have determined a significant difference in genotypes of rs7895833 in SIRT1 gene. Especially, the AG genotype was observed more in the group with vitiligo. It was determined that the rs7895833 G allele had a protective effect in terms of vitiligo (p=0.001). Intergene interaction analysis was also performed by in silico method, and it was shown that SIRT 1 is co-expressed with 16 genes and shares an area with only 12 genes physically interacting with 19 genes. We showed gene ontology and pathway analyzed with all relevant genes. It was determined that especially apoptosis and systemic sclerosis were associated with these genes. Conclusion: The SIRT1 rs7895833 SNP genotype and allele frequencies of vitiligo patients are significantly different from healthy controls. Our study shows that the rs7895833 polymorphism of the SIRT1 gene may be associated with vitiligo susceptibility. Considering the role of sirtuin and related genes, especially in the apoptotic pathway, its effect on vitiligo can be further investigated to elucidate the molecular aspect of the disease.