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According to a new study, a cytokine known as TWEAK works along with two other proteins—tumor necrosis factor (TNF) and interleukin-17 (IL-17)—to trigger skin inflammation in individuals suffering from psoriasis.
Mice having a keratinocyte-specific deletion of the receptor for the cytokine TWEAK, Fn14, display reduced skin inflammation upon chemical induction, including decreased epidermal hyperplasia and less expression of psoriasis signature genes. Based on this finding and transcriptomic analysis of human keratinocytes, Michael Croft, PhD, and his team have shown TWEAK works together with the known cytokines TNF or IL-17 in provoking inflammation in psoriasis. The study shows targeting TWEAK could offer an alternative approach to treating the disease.
About 7.5 million Americans suffer from psoriasis, an autoimmune disease that shows up as patches of red, inflamed skin and painful, scaly rashes.
About 7.5 million Americans suffer from psoriasis, an autoimmune disease that shows up as patches of red, inflamed skin and painful, scaly rashes. Although there are effective treatments for psoriasis, not everyone responds to these therapies-;and for many, the relief is temporary.