Periodontal clinical measures, on salivary interleukin 2, interleukin 6 and secretory immunoglobulin A levels and the Psoriasis Area and Severity Index (PASI) scores were evaluated at baseline and on the 8th week in control and test groups.
Proteomic panels revealed IL-6 as a top differentially expressed cytokine in psoriasis with pathway analysis highlighting IL-1β ( Z score 3.7; P=1.02×10<sup>-23</sup>) as an upstream activator of the observed upregulated proteins.
Proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are elevated in both psoriasis and depression, indicating that the inflammatory process may be involved in the progression of both diseases.
Anti-IL-6 therapies, however, which are effective for rheumatoid arthritis, are either ineffective for psoriasis or can induce new-onset psoriasis-like disease.Fritz et al. provide a potential explanation for these clinical observations by examining IL-17C-driven psoriasis-like disease in mice with an IL-6-deficient genetic background.
These preclinical findings may provide insight into why patients with arthritis being treated with IL-6 inhibitors develop new onset psoriasis and why IL-6 blockade for the treatment of psoriasis has not been clinically effective.
They accepted the treatment of NB-UVB and the following data were collected: serum levels of IL-17 (interleukin), TNF-α (tumor necrosis factor) and IL-6, Psoriasis Area and Severity Index (PASI) scores before and after 10 sections of NB-UVB treatment.Significant PASI improvement was observed in psoriatic patients without MS after 10 sections of phototherapy, while patients with MS showed a less improvement (P < .001).
A single treatment with the liquid crystalline nanodispersion carrying IL-6 siRNA for 6h was able to reduce the extracellular IL-6 levels by 3.3-fold compared with control treatment in psoriasis skin model.
We conclude that the IL6 -174G>C polymorphism can be a marker of susceptibility to psoriasis, with an almost twofold increased risk of the disease in individuals carrying the GG genotype; however, it was not associated with treatment response to topical and/or NB-UVB therapy.
This study aims to assess whether the association between the non-susceptibility allelic variants of IL12B single-nucleotide polymorphism (SNPs) rs3212227 and rs6887695, IL23R SNPs rs11209026 and rs7530511, IL6 SNP rs1800795 and HLA-Cw6 could be correlated with decreased risk for psoriasis.
The modulation by LL-37 of the keratinocyte proinflammatory responses induced by cytokine milieus and dsRNA suggests novel roles for LL-37 in skin inflammation such as the promotion of IL17/IL-22/IL-6-associated psoriasis and suppression of TSLP-associated atopic dermatitis.
We found that there were a three-way interaction among IL21, CCR4 and TNF(χ(2) = 5.02(1), P = 0.025) and three pair-wise gene-gene interactions between IL12RB1 and CCR4(χ(2) = 11.66(4), P = 0.0201), IL22 and CCR4 (χ(2) = 11.97(4), P = 0.0176), IL12RB1 and IL6 (χ(2) = 7.31(1), P = 0.0069) in psoriasis.
To examine whether the G or the C allele, at position -174 in the promoter of IL-6, influences the relationships between body weight, body composition, and therapeutic response to TNF-α blockers in psoriasis.