"We have developed a mouse model that exhibits all the major features of human psoriatic lesions and shown we can reverse those steps," said John DiGiovanni, Ph.D., the study's principal investigator and director of M. D. Anderson's Department of Carcinogenesis. "We may have found an entirely new treatment option for psoriasis."
The study, which appears in the January 2005 issue of the journal Nature Medicine, available on-line Dec. 12, shows a protein called STAT3 is a crucial initiator of psoriasis and must be present and activated for psoriasis to develop in their mouse model.
Psoriasis is a chronic condition in which patches of skin become inflamed and develop itchy red, flaky scales. Areas of the body most affected include the scalp, elbows, knees, and lower back. Psoriasis affects about two percent of people worldwide, with men and women equally susceptible. Current treatment for psoriasis focuses on reducing inflammation and slowing down the rapid growth and shedding of skin cells called keratinocytes. There is no effective curative treatment for the underlying condition, according to DiGiovanni.
"There has been an ongoing controversy about whether the primary defect in psoriasis is in the immune system or in the keratinocytes," says DiGiovanni. "We may have found the link - the change in keratinocytes that cooperates with the immune system cells necessary for development of human psoriasis."
The researchers became interested in STAT3 when they learned it was associated with
Contact: Julie A. Penne
University of Texas M. D. Anderson Cancer Center