IN-VITRO CYTOKINE MODULATION OF INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION ON SYSTEMIC-SCLEROSIS NORMAL DERMAL FIBROBLASTS

被引:17
作者
CHO, MM
JIMENEZ, SA
JOHNSON, BA
HARLOW, LA
BURROWS, JC
KOCH, AE
机构
[1] THOMAS JEFFERSON UNIV, JEFFERSON MED COLL, PHILADELPHIA, PA 19107 USA
[2] LAKESIDE VET ADM MED CTR, CHICAGO, IL USA
[3] NORTHWESTERN UNIV, SCH MED, DEPT MED, CHICAGO, IL 60611 USA
关键词
SYSTEMIC SCLEROSIS; CELL ADHESION; FIBROBLAST; SKIN; LEUKOCYTES;
D O I
10.1159/000163881
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Our objective was to study the regulation of intercellular adhesion molecule-1 (ICAM-1) expression by cytokines on cultured fibroblasts obtained from systemic sclerosis and normal skin. ICAM-1 expression on dermal fibroblasts obtained from diffuse systemic sclerosis patients with early disease(less than or equal to 2 years) and normal dermal fibroblasts incubated with and without cytokines was measured by radioimmunoassay and flow cytometry. Systemic sclerosis dermal fibroblasts expressed lower basal levels of ICAM-1 than did normal dermal fibroblasts. Both the normal and systemic sclerosis dermal fibroblasts increased their cell surface expression of ICAM-1 in response to interleukin-1 beta (IL 1 beta), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma(IFN-gamma) in a dose-dependent fashion. Systemic sclerosis dermal fibroblasts appeared to be hyperresponsive to IL-1 beta, TNF-alpha, and IFN-gamma. ICAM-1 expression in response to cytokine stimulation increased to a greater degree on systemic sclerosis compared to normal dermal fibroblasts. The enhanced ICAM-1 expression may play a role in the retention of leukocytes involved in systemic sclerosis skin lesions.
引用
收藏
页码:73 / 81
页数:9
相关论文
共 51 条
[11]   GAMMA-INTERFERON IS THE LYMPHOKINE AND BETA-INTERFERON THE MONOKINE RESPONSIBLE FOR INHIBITION OF FIBROBLAST COLLAGEN PRODUCTION AND LATE BUT NOT EARLY FIBROBLAST PROLIFERATION [J].
DUNCAN, MR ;
BERMAN, B .
JOURNAL OF EXPERIMENTAL MEDICINE, 1985, 162 (02) :516-527
[12]  
DUSTIN ML, 1992, J IMMUNOL, V148, P2654
[13]  
DUSTIN ML, 1986, J IMMUNOL, V137, P245
[14]   COLLAGEN IN CELLULAR AND FIBROTIC STAGES OF SCLERODERMA [J].
FLEISCHMAJER, R ;
GAY, S ;
MEIGEL, WN ;
PERLISH, JS .
ARTHRITIS AND RHEUMATISM, 1978, 21 (04) :418-428
[15]   CELLULAR INFILTRATES IN SCLERODERMA SKIN [J].
FLEISCHMAJER, R ;
PERLISH, JS ;
REEVES, JRT .
ARTHRITIS AND RHEUMATISM, 1977, 20 (04) :975-984
[16]   ALTERATION OF SUBCUTANEOUS TISSUE IN SYSTEMIC SCLERODERMA [J].
FLEISCHMAJER, R ;
DAMIANO, V ;
NEDWICH, A .
ARCHIVES OF DERMATOLOGY, 1972, 105 (01) :59-+
[17]   CHARACTERIZATION OF A SPONTANEOUS DISEASE OF WHITE LEGHORN CHICKENS RESEMBLING PROGRESSIVE SYSTEMIC-SCLEROSIS (SCLERODERMA) [J].
GERSHWIN, ME ;
ABPLANALP, H ;
CASTLES, JJ ;
IKEDA, RM ;
VANDERWATER, J ;
EKLUND, J ;
HAYNES, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1981, 153 (06) :1640-1659
[18]   MODULATION OF LEUKOCYTE ADHESION MOLECULES, A T-CELL CHEMOTAXIN (IL-8) AND A REGULATORY CYTOKINE (TNF-ALPHA) IN ALLERGIC CONTACT-DERMATITIS (RHUS DERMATITIS) [J].
GRIFFITHS, CEM ;
BARKER, JNWN ;
KUNKEL, S ;
NICKOLOFF, BJ .
BRITISH JOURNAL OF DERMATOLOGY, 1991, 124 (06) :519-526
[19]  
ISHIKAWA O, 1992, J RHEUMATOL, V19, P1202
[20]   CHRONIC GRAFT-VERSUS-HOST DISEASE (GVHD) AS A MODEL FOR SCLERODERMA .1. DESCRIPTION OF MODEL SYSTEMS [J].
JAFFEE, BD ;
CLAMAN, HN .
CELLULAR IMMUNOLOGY, 1983, 77 (01) :1-12