These medications target various cytokines responsible for psoriasis manifestations such as tumor necrosis factor (TNF-α), interleukin-12, interleukin-23, and interleukin-17.
TNF-α-238 G/A, -308 G/A and -857 C/T polymorphisms could be used to identity individuals with elevated susceptibility to psoriasis in certain populations.
The pro-inflammatory cytokine, TNF-α, which plays a major role in the development and persistence of diseases such as Crohn's disease, psoriasis, psoriatic arthritis, and rheumatoid arthritis, is the basis for the use of anti-TNF-α therapies.
Tumor necrosis factor (TNF) inhibitors account for a large proportion of drugs used to treat psoriasis and are indicated first-line options in certain settings.
In PS, there are enhanced type I interferon (IFN), angiogenesis, and over-expression of several proinflammatory cytokines, such as tumor necrosis factor and interleukin (IL)-1 family members generated by several immune cells including MCs.
On the other hand, inhibition of IL-12-IL-23, as compared with inhibition of TNF, has greater efficacy for psoriasis, comparable efficacy for peripheral arthritis, but was ineffective in studies of axial spondyloarthritis.
Biologic therapies targeting tumor necrosis factor have revolutionized treatment of immune-mediated inflammatory diseases such as psoriasis, but optimal dosing and appropriate use of therapeutic drug monitoring are not yet fully understood.Wilkinson et al. explore these questions in a real-world psoriasis cohort on adalimumab monotherapy, defining a therapeutic range and finding value in early measurement for predicting clinical response.
Tumor necrosis factor inhibitors decrease the risk of cardiovascular events in moderate to severe psoriasis, but the association between their effects on endothelial function and those on skin lesions has not been well studied.
A significant increase in PASI 75 (RR: 11.65; 95% CI: 9.01-15.06), PASI 90 (RR: 21.74; 95% CI: 14.28-33.10), PASI 100 (RR: 31.56; 95% CI: 14.66-67.96), PGA 0/1 (OR: 23.21; 95% CI: 14.61-36.89), and DLQI 0/1 (RR: 10.29; 95% CI: 7.52-14.09) was identified for anti-IL-23p19 mAb vs. placebo, and PASI 75 (RR: 1.25; 95% CI: 1.18-1.32), PASI 90 (OR: 2.56; 95% CI: 2.13-3.09), PASI 100 (OR: 2.38, 95% CI: 1.89-2.99), and DLQI 0/1 (RR: 1.33; 95% CI: 1.20-1.47) vs. tumour necrosis factor (TNF) antagonists for the treatment of psoriasis.
Over the last decades, research advances in understanding the role of tumor necrosis factor alpha (TNF α) and other cytokines in the pathogenesis of psoriasis have driven the introduction of biologic agents targeting specific immune mediators in everyday clinical practice.
<b>Conclusions:</b> In a long-term real-life setting, drug survival of UST is better than that of TNF-a inhibitors for both biologic-naive and biologic-experienced patients with psoriasis.
Blocking of CXCL16 expression by effective treatment of psoriasis patients with tumor necrosis factor-α blockers further supported the pathogenic role of this chemokine.
Tumor necrosis factor α (TNFα) is a proinflammatory cytokine, and elevated levels of TNFα in serum are associated with various autoimmune diseases, including rheumatoid arthritis (RA), ankylosing spondylitis (AS), Crohn's disease (CD), psoriasis, and systemic lupus erythaematosus.
T helper (Th) cytokines in psoriasis upregulate keratin (K)17, which modulates TNF-α transduction, leading to vascular adhesion molecule upregulation and lymphocytic extravasation.