Inhibiting IL-17 Activity to Treat Psoriatic Disease

Tiago Torres, MD, PhD, discusses how inhibition of the cytokine IL-17 is critical for treating psoriatic disease. Dr Torres is professor of dermatology at the Instituto de Ciências Biomédicas Abel Salazar at the University of Porto in Porto, Portugal. 

Transcript
Dr Torres:  The IL-23/IL-17 immunological pathway has been shown to be a crucial factor for psoriatic inflammation. The IL-23 regulation T_H17 cells both help cytotoxic. TH17 cells produce high levels of IL-17A and also IL-17F, which create a self-amplifying feed-forward inflammatory response that consequently develop and maintain the psoriatic disease.

This knowledge led to development of highly selective therapies that target these cytokines. These therapies have shown to be highly effective in treating psoriasis. We're talking about ixekizumab and secukinumab, which target IL-17A; brodalumab, which targets the receptor of IL-17; and more recently, bimekizumab that function as a dual inhibitor of IL-17A and IL-17F.

IL-17 inhibition has shown to be highly effective, more effective than TNF inhibition and also, ustekinumab, IL-12/IL-23 inhibition. With high rates of complete or almost complete skin clearance, very important also, a very rapid onset of response, and also, has been shown to be effective for psoriatic arthritis.

The safety profile of IL-17 inhibition is also very favorable with mucocutaneous candida infection representing the most common safety issue with these drugs, although most cases are mild to moderate, do not require discontinuation, and are easily treated. It appears that IL-17 inhibition may be detrimental for inflammatory bowel disease.

In summary, IL-17 inhibition has been shown to be highly effective and safe in treatment of psoriasis and of course, are important treatment weapons that we have at our hands.