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Study links key protein to psoriasis
Research on mice could lead to effective treatment
Updated: 12:39 p.m. ET Dec. 13, 2004WA****NGTON - Researchers said
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.
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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."
Research opens door to new treatment
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.
Copyright 2004 Reuters Limited. All rights reserved. Republication or
redistribution of Reuters content is expressly prohibited without the
prior written consent of Reuters.
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