Interleukin (IL)-36 does appear to play an important role in the development of psoriasis, and blocking it could be a safe, effective approach to therapy, researchers conclude in a paper published in Science Translational Medicine (Oct. 11, 2017; 9(411): eaan2514).
The authors note that IL–36α, IL-36β, and IL-36γ are known to be innate mediators of acute epithelial inflammation. To investigate the potential role of these cytokines in psoriasis, they first identified the genes in primary human keratinocytes which are switched on by IL-36 cytokines. This allowed them to find a significant correlation between those genes and the genes which are up-regulated in plaque psoriasis.
Follow-up in vivo and ex vivo studies that tested either a neutralizing antibody or a recombinant antagonist to block IL-36 receptors showed strong anti-inflammatory effects on psoriatic skin.
In a press release, lead author Dr. Francesca Capon, who led the study at King’s College London said: “There was already some evidence to suggest that IL-36 played a significant role in psoriasis. Having confirmed this was the case, the question for us was whether we could block this molecule without posing a risk to patients.”
Dr. Capon is a senior lecturer in the department of medical and molecular genetics.
To investigate the safety of IL-36 blockade in psoriasis, Dr. Capon and her team used data from the Born in Bradford (BiB) project, which tracked the health of 13,500 children and their parents. From that cohort, 12 women were identified who carried a genetic defect that naturally blocked IL-36.
“After a series of tests carried out by Dr. Satveer Mahil at St. John’s Institute of Dermatology [at King’s College, London], we determined that the lack of IL-36 activation had not had an adverse effect on their health which suggests it would be safe to block this molecule in patients with psoriasis,” said Dr. Capon.
Medical technology to block IL-36 already exists, the authors note in the press release.
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