Expert dermatologist Dr Linda Stein Gold discusses the pathophysiology of psoriasis as target for treatment.
Linda Stein Gold, MD: Traditionally we've used broad immunosuppressants to treat our psoriasis patients, but as we've come to understand the pathogenesis of disease, we're able to…target our treatments to better hit those abnormalities in the immune system, which are underlying the pathogenesis of disease. We know that the inflammatory pathway that drives psoriasis is…modulated by proinflammatory cytokines and cytokine signaling. So we don't know exactly what starts off this whole process, but something happens that causes keratinocytes to release antimicrobial peptides and pro-inflammatory signals. These call into action these inflammatory cells, including plasma dendritic cells. They secrete a type 1 interferon, which activates a number of cells, including myeloid dendritic cells, and this cell secrete IL-23 and IL-12. Now, it's IL-23 that…simulates the differentiation of T cells to form TH-17 cells. And these TH-17 cells produce IL-17, and IL-17 is that cytokine that's important in the end organ damage. And if we think of the end organs being the skin and the joints, this causes the signs and symptoms of psoriasis. So, when we take a step back and look at what is the key axis that really drives psoriasis and psoriasis pathogenesis, we understand that it's this IL-23 and IL-17 pathway that really is at the core of psoriasis pathogenesis.
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