Abstract
Psoriasis is a common, chronic, and autoimmune skin disease in which dysregulation of immune cells, particularly T cells, is thought to play an important role in the pathogenesis. Cytotoxic T lymphocyte antigen-4 (CTLA-4) expressed only on activated T cells is an immunoregulatory molecule and plays a role in the pathogenesis of autoimmune disorders. We aimed to determine whether CTLA-4 gene polymorphisms are associated with development and/or clinical features of psoriasis vulgaris (Pv). Genotyping of SNPs (−318C>T, +49A>G, and CT60A>G) in CTLA-4 gene was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 103 Pv patients and 102 controls. No statistically significant associations were detected in any of the investigated genetic models for the −318C>T polymorphism. The genotype distributions of +49A>G and CT60A>G were associated with Pv development. In haplotype analysis, while frequency of CAA haplotype was significantly higher in the control group, frequencies of CGG and CAG haplotype were significantly higher among the patients. However, all of CTLA-4 polymorphisms and haplotypes do not have an effect on severity and onset age of Pv. In conclusion, the +49A>G and CT60A>G polymorphisms may be risk factors for Pv development. Furthermore, CGG and CAG haplotypes may contribute to Pv development, while CAA haplotype may be protective against Pv.
Highlights
Psoriasis is a common inflammatory skin disease that affects approximately 125 million people globally [1]
Our goal was (i) to investigate whether the Cytotoxic T lymphocyte antigen-4 (CTLA-4) gene polymorphisms are related to the development of psoriasis vulgaris (Pv) and (ii) to detect whether the CTLA-4 gene polymorphisms have an impact on the clinical features of P. vulgaris such as onset age and severity
To determine the association of CTLA-4 gene polymorphisms with the clinical features of Pv, the patients were divided into two groups according to the severity of disease (PASI < 12 group and Psoriasis Area and Severity Index (PASI) ≥ 12 group) and assigned into two groups according to the onset of disease (Table 1)
Summary
Psoriasis is a common inflammatory skin disease that affects approximately 125 million people globally [1]. Psoriasis has begun to be defined as a disease spectrum or systemic disease because of abovementioned concomitant comorbidities. As a result, it requires lifelong treatment [16]. The molecular pathogenesis of the disease is still poorly understood, it is generally agreed that psoriasis is triggered by some environmental factors such as stress, infections, trauma, and drugs with a genetic background [17]. The common view about the molecular pathogenesis of the disease is that alterations in the complex interactions between T lymphocytes, dendritic cells, macrophages, mast cells, neutrophils, keratinocytes, cytokines, and chemokines cause psoriasis, and this wise
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