Researchers at the University of California, San Diego, have identified a secreted intestinal antimicrobial protein (REG3A) that promotes skin keratinocyte proliferation. Understanding its mechanism of action may lead to new treatments that improve wound healing and reduce the abnormal epithelial profileration of psoriasis.
The researchers, led by Richard Gallo, MD, were seeking to identify the inflammatory processes that trigger epithelial proliferation. According to the study—which appears in Immunity (online June 21, 2012)—the researchers were able to show that regenerating islet-derived protein 3-alpha (REG3A) is “highly expressed in keratinocytes during psoriasis and wound repair and in imiquimod-induced psoriatic skin lesions. The expression of REG3A by keratinocytes is induced by interleukin-17 (IL-17) via activation of keratinocyte-encoded IL-17 receptor A (IL-17RA)…These findings reveal that REG3A, a secreted intestinal antimicrobial protein, can promote skin keratinocyte proliferation and can be induced by IL-17. This observation suggests that REG3A may mediate the epidermal hyperproliferation observed in normal wound repair and in psoriasis.”
Dr. Gallo, et al, posit that a drug developed to inhibit REG3A expression “could represent a more targeted way to treat psoriasis without the systemic immunosuppression problems of current treatments. Conversely, a drug that stimulates or mimics REG3A could boost cell growth and improve wound healing.”