Transforming growth factor-β1 gene polymorphism in psoriasis vulgaris

Abstract

BackgroundIncreased transforming growth factor beta 1 (TGF-β1) in the epidermis and serum has been found in psoriatic patients. The mechanism for this increase remains unclear.ObjectiveTo study the TGF-β1 gene polymorphism at codon 10 and its relation to psoriasis susceptibility in a sample of Egyptian patients.Materials and methodsThis cross-sectional study involved 70 patients with psoriasis vulgaris and 100 age- and sex- comparable healthy volunteers as a control group. Genomic DNA was prepared from peripheral blood lymphocytes from all subjects using QIAamp DNA mini kit (QIAGEN Inc., Germany). The TGF-β1 polymorphism was genotyped by PCR-based restricted fragment length polymorphism (PCR-RFLP) analysis. Amplification of codon 10, located in exon 1 of TGFβ1 gene was done through PCR reaction using gene-specific primers.ResultsStatistically significant difference was found between psoriasis patient and controls as regards TGF-β1 (T869C) polymorphism (P=0.045). The presence of TT genotype was associated with a 3-fold risk of psoriasis compared to CC genotype (P=0.016, OR: 3.13 95% CI: 1.24–7.88). T allele was significantly more frequent in psoriasis patients (P=0.017). TGF-β1 gene mutation was significantly higher among psoriasis patients with positive family history (P=0.007).ConclusionTGF-β1 gene polymorphism at codon 10 (T869C) is significantly associated with susceptibility to psoriasis in Egyptian patients. This polymorphism is more common in patients with a positive family history of psoriasis.

The Influence of Adalimumab and Cyclosporine A on the Expression Profile of the Genes Related to TGFβ Signaling Pathways in Keratinocyte Cells Treated with Lipopolysaccharide A

“…It plays an important role in the induction and pathogenesis of psoriasis, during which its elevated level is observed [ 11 , 12 ]. Depending on the biological context, including changes in the level of secretion of interleukins (IL), IL-1, IL-6, and IL-8, TGF β may inhibit or promote the proliferation of keratinocytes [ 13 , 14 ]. Despite observations [ 15 , 16 ], including ours [ 17 , 18 ], that TGF β may become a complementary molecular marker in the diagnosis of the severity of the psoriatic process [ 15 – 18 ], the exact mechanism of its action is still not fully understood.…”

<p>Circulating Cell-Free DNA as Inflammatory Marker in Egyptian Psoriasis Patients</p>

“…However, there are several studies are available dealing with other factors that play roles in the pathogenesis, their correlation to disease severity or treatment of psoriasis. [10][11][12] There are some studies also concerning the different protocols for the management of psoriasis at Kasr Al-Ainy's Psoriasis Unit, Cairo, 13 either topical and systemic therapies or biological therapies. 14 We hypothesized that the inflammatory and hyperproliferative features of psoriasis may be associated with increased levels of CFD that may provide a new inflammatory marker to monitor psoriasis, its severity and treatment in Egyptian patients.…”

Assessment of transcriptional activity genes associated with the IL‐17 signaling pathway in skin fibroblasts under the influence of adalimumab

“…Therefore, it is extremely important to look for new, complementary molecular markers that allow to observe the loss of sensitivity to treatment at the level of molecular changes that are ahead of phenotypic changes (Wcisło‐Dziadecka, Grabarek, Brzezińska‐Wcisło, & Mazurek, ). Due to the complex immunopathogenesis and involvement of a large number of signaling pathways in the initiation and development of psoriatic lesions (Albanesi, ), it seems that marker systems should be sought not only among genes of signaling cascades inhibited by a given drug (Singh & Argáez, ; El‐hadidi et al, ; Teng et al, ).…”

“…Anti-TNF therapy is one of the most effective forms of biological treatment used in the treatment of moderate to severe psoriasis . It is used when conventional methods of treatment did not allow an adequate response to treatment Reich, Szepietowski, et al, 2018 (Albanesi, 2019), it seems that marker systems should be sought not only among genes of signaling cascades inhibited by a given drug (Singh & Argáez, 2018;El-hadidi et al, 2018;Teng et al, 2015).…”