Psoriasis, a chronic skin disorder caused by the immune system, affects 1%-2% of white individuals. Although there are a number of treatments, the chronic recurrent nature of the disorder means more efficient therapies are being sought. Work in a mouse model of psoriasis-like inflammation, by Joshua Farber and colleagues, at the National Institute of Allergy and Infectious Diseases, Bethesda, has provided new insight into the immune mechanisms that likely underlie psoriasis and identified a potential new drug target.
In the study, when the soluble immune molecule IL-23 was injected into the ears of normal mice the ears developed psoriasis-like inflammation. By contrast, no inflammation developed when IL-23 was injected into the ears of mice lacking the protein CCR6. As immune cells known as Th17 cells express CCR6, initial analysis focused on these cells. Consistent with a role for these cells in the IL-23–induced psoriasis-like inflammation, injection of the immune molecule IL-22 (which is produced by Th17 cells) into the ears of normal and CCR6-deficient mice induced equivalent inflammation.
However, further analysis indicated that the IL-22 did not come from Th17 cells, rather it came from a non–T cell source. The authors therefore conclude that CCR6 is essential for IL-23–induced, IL-22–mediated psoriasis-like inflammation, which initially develops in a T cell–independent manner, and suggest that CCR6 might be a therapeutic target for the treatment of psoriasis.
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