Psoriasis patient skin has elevated IL-6 and IL-6 receptor is present in human coronary atheroma, supporting a link between skin and distant vessel disease in patient tissue.
Regarding IL-6, in patients with geographic tongue and psoriasis cases the staining was stronger than in patients with geographic tongue without psoriasis cases.
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.
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.
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.
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.
Therefore, these results suggest a novel role of IGF-II in psoriasis possibly by inducing IL-6 through the activation of NFkappaB mediated by downregulation of IkappaB.
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.
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.
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.
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.
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.
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.
Elevated levels of IL-6 are observed in human body fluids during acute and chronic infections, neoplasia, autoimmune diseases, and psoriasis and following third-degree burns.
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.