|
||
Journal of Experimental Medicine, Vol 168, 941-948, Copyright © 1988 by Rockefeller University Press
ARTICLES |
AB Gottlieb, AD Luster, DN Posnett and DM Carter
Laboratory of Immunology, Rockefeller University, New York.
The pathologic features of psoriatic plaques are inflammation and increased epidermal turnover. IP-10, a cytokine the expression of which is induced by gamma-interferon, is a member of a family of soluble mediators with inflammatory and growth-promoting activities. IP-10 protein was detected in keratinocytes and the dermal infiltrate from active psoriatic plaques using an affinity-purified rabbit anti-IP-10 antibody in immunoperoxidase studies. Successful treatment of active plaques decreased IP-10 expression in plaques. These results were corroborated by Northern blot analysis with an IP-10 cDNA probe. We have previously detected activated T cells and HLA-DR keratinocytes in active psoriatic plaques. Since IP-10 is detected in delayed cellular immune responses, the present study further points to the role of ongoing cellular immune responses in the pathogenesis of psoriasis.
This article has been cited by other articles:
| TABLE OF CONTENTS |
|