Mice study opens door to psoriasis treatment

Researchers said on Sunday they may have discovered what causes psoriasis, a common and irritating skin ailment, and said their findings may open the way to an effective treatment.

They found that it takes a combination of a protein called STAT3 and an active immune system to cause psoriasis, which experts estimate affects as much as 2 percent of the population.

Their finding suggests that psoriasis may start with an over-enthusiastic attempt by the body to heal wounds.

And the researchers at The University of Texas M. D. Anderson Cancer Center made a skin cream that blocked the process that leads to psoriasis in mice.

"We may have found an entirely new treatment option for psoriasis," said M.D. Anderson's John DiGiovanni, who led the study.

"We have developed a mouse model that exhibits all the major features of human psoriatic lesions and shown we can reverse those steps."

Psoriasis is a chronic condition in which patches of skin become inflamed and become itchy, red and flaky. There is no good treatment, although symptoms can be alleviated.

The disease involves skin cells called keratinocytes that grow too fast and too abundantly.

"There has been an ongoing controversy about whether the primary defect in psoriasis is in the immune system or in the keratinocytes," DiGiovanni said in a statement.

"We may have found the link - the change in keratinocytes that cooperates with the immune system cells necessary for development of human psoriasis."

Writing in the journal Nature Medicine, the researchers said they looked at STAT3, a protein involved in wound healing and the development of skin cancer.

Activated STAT3 is essential for wound healing. When the healing process is complete, normal STAT3 returns to its inactive form. But when it fails to turn off, the wound healing process continues and skin cells proliferate.

DiGiovanni's team first looked for activated STAT3 in the skin of psoriasis patients and found high levels of activated STAT3 in psoriasis lesions in 19 of 21 of them.

They bred a mouse in which STAT3 is always turned on in the keratinocyte skin cells, and these mice always developed psoriasis.

The researchers then developed a solution containing a small piece of DNA called an oligonucleotide, which was designed to prevent STAT3 from activating genes.

It helped clear up the lesions in the mice.

"This study opens the door to a whole new kind of therapy for psoriasis," said DiGiovanni.

SOURCE: Nature Medicine, December 13, 2004.