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Single gene may prevent chronic psoriasis by switching off inflammation

Researchers from the Karolinska Institutet in Stockholm, Sweden, have identified a gene that appears to play a role in shutting off skin inflammation, representing a potential target for managing psoriasis, according to a paper published online ahead of print in The Journal of Allergy and Clinical Immunology (Aug. 24, 2016).

The gene the group identified is responsible for the production of a micro-RNA protein named miR-146a. Earlier research from the Karolinska Institutet group has previously shown that miR-146a exists in skin cells and has altered activity in psoriasis.

“The absence of miR-146a causes more pronounced skin inflammation, which also develops more quickly,” Enikö Sonkoly, PhD, associate professor of dermatology at Karolinska Institutet’s Department of Medicine, said in a press release. “In mice lacking miR-146a we see a slower and incomplete healing process.”

In the paper, the authors conducted a genetic analysis of 1,546 psoriasis patients and 1,526 controls and found a particular variant of the miR-146a gene was protective against psoriasis.

The greater level of protection was seen in individuals lacking the HLA-Cw6 gene, which is an important psoriasis risk factor, the authors write. In this group the risk of psoriasis was halved in those individuals who had the protective variant of miR-146a.

Investigations on a mouse model showed the miR-146a gene plays a strong role in preventing chronicity by switching off inflammation in the skin. The micro-RNA also modulates the response of skin cells to the cytokine IL-17, which is targeted by some psoriasis management therapies. When the authors injected synthetic miR-146a into mice who had artificially induced psoriasis-like symptoms, the micro-RNA effectively alleviated the skin inflammation.

“Our results suggest that the modulation of microRNA levels by, say, delivering synthetic microRNA into the cells, could constitute a new method of psoriasis therapy,” said Dr. Sonkoly.

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