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THE CYTOKINE NETWORK IN LESIONAL AND LESION-FREE PSORIATIC SKIN IS CHARACTERIZED BY A T-HELPER TYPE-1 CELL-MEDIATED RESPONSE
Author(s): UYEMURA K, YAMAMURA M, FIVENSON DF, MODLIN RL, NICKOLOFF BJ
Source: JOURNAL OF INVESTIGATIVE DERMATOLOGY    Volume: 101    Issue: 5    Pages: 701-705    Published: NOV 1993  
Times Cited: 266     References: 31     
Abstract: As a psoriatic lesion develops at sites of previously uninvolved skin, cytokines and their subsequent induction of various adhesion molecules may play important pathophysiologic roles. To further define the cytokine network in psoriasis, biopsies were obtained from both lesional skin and lesion-free skin of individuals with psoriasis and compared to normal skin biopsies from control subjects. Each biopsy was analyzed using polymerase chain reaction for expression of cytokines and immunostaining to detect adhesion molecules. The results indicate that psoriatic lesions have a type 1 cytokine profile (i.e., interleukin[IL]-2, interferon[IFN]-gamma, and tumor necrosis factor[TNF]-alpha), without a significant component of type 2 cytokines (i.e., IL-4, IL-5, and IL-10) accompanied by aberrant expression of endothelial cell leukocyte adhesion molecule (ELAM)-1 and vascular cell adhesion molecule (VCAM)-1 on dermal endothelial cells, and ICAM-1 on epidermal keratinocytes. Four of five lesion-free biopsies from psoriatic patients had prominent cytokine mRNA expression compared with skin from normal donors (particularly TNF-alpha, IL-1alpha, IL-1beta, with lesser increases in IFN-gamma and granulocyte/macrophage colony-stimulating factor [GM-CSF]), which was accompanied by aberrant adhesion molecule expression in the same four samples. We conclude that a particular T-cell population producing type 1 cytokines accumulates in psoriatic lesions. In addition, clinically lesion-free skin is characterized by increased levels of various cytokine mRNAs, and aberrant adhesion molecule expression in both dermal and epidermal compartments.
Document Type: Article
Language: English
Reprint Address: UYEMURA, K (reprint author), UNIV CALIF LOS ANGELES, SCH MED, DIV DERMATOL, 52-121 CHS, 10833 LE CONTE AVE, LOS ANGELES, CA 90024 USA
Addresses:
1. UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, LOS ANGELES, CA 90024 USA
2. UNIV MICHIGAN, SCH MED, DEPT PATHOL, ANN ARBOR, MI 48104 USA
Publisher: BLACKWELL SCIENCE INC, 238 MAIN ST, CAMBRIDGE, MA 02142
Subject Category: Dermatology
IDS Number: ME694
ISSN: 0022-202X
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