English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Address for correspondence: Michał Sobjanek MD, PhD, Department of Dermatology, Venereology and Allergology, Medical University of Gdansk, 1a Kliniczna St, 80-402 Gdansk, Poland, phone: +48 607 039 729, e-mail: sobjanek@wp.pl Received: 8.01.2016, accepted: 20.04.2016. The ethiopathogenesis of psoriasis is complex, multifactorial and still not well understood. Nowadays, the systemic, inflammatory and autoimmunological aspects of psoriasis are being emphasized [1]. Toll-like receptors (TLR) are characterized as patternrecognition receptors, which are capable of potently activating various cell types. Toll-like receptors downstream signalling pathways lead to the production of a wide range of immune stimulatory cytokines and chemokines. Aberrant activation of TLR may result in an unrestricted inflammatory response, so the receptors may play a role in the development of inflammatory and autoimmune disorders [2]. TLR1, 2 and 5 are constitutively expressed on the normal keratinocytes [3]. TLR1 and TLR2 expression is further upregulated in psoriatic lesions [3, 4]. Seung et al. found a higher expression of TLR4 in guttate psoriasis compared to the plaque type and controls [5]. Moreover, TLR5 and TLR9 were upregulated by transforming growth factor α (TGF-α) in psoriatic keratinocytes [6]. In another study, Begon et al. showed the expression of tumor necrosis factor α (TNF-α) and interleukin (IL)-8 induced by the TLR2, 3 and 4 signalling pathway via nuclear factor κB (NF-κB) nuclear translocation in psoriatic keratinocytes [7]. In the light of these facts, TLR genes seem to be interesting gene candidates involved in psoriasis pathogenesis. In this study we clarified the effect of Arg753Gln TLR2 and –1237 T/C TLR9 gene polymorphisms on the risk and the clinical manifestation of psoriasis. The study group consisted of 175 unrelated patients with psoriasis vulgaris and 170 healthy, unrelated, ageand sex-matched volunteers. The mean Psoriasis Area Severity Index (PASI) was 16.9; PASI > 10 was observed in 90 patients. In the study group there were 121 (78.1%) patients with early onset (< 40 years) and 39 with late onset psoriasis (≥ 40 years). The gene polymorphisms were analyzed using the amplification refractory mutation system polymerase chain reaction method (ARMSPCR). There was no statistically significant association between genotype and allele frequencies in psoriatic patients in comparison with controls (Table 1). However, the presence of allele G in Arg753Gln TLR2 polymorphism was statistically more frequent in the group with late onset psoriasis in comparison with early onset psoriasis (100% vs. 96.2%; p = 0.0127). The presence of allele T in –1237 T/C TLR9 polymorphism was more common in the group of early onset psoriasis (86.3% vs. 73.8%; p = 0.0086) and their presence increases more than twice the risk of the development of this type of the disease The significance of Toll-like receptor (TLR) 2 and 9 gene polymorphisms in psoriasis