IL-10 augments the IFN-γ and TNF-α induced TARC production in HaCaT cells:: a possible mechanism in the inflammatory reaction of atopic dermatitis

被引:54
作者
Vestergaard, C
Kirstejn, N
Gesser, B
Mortensen, JT
Matsushima, K
Larsen, CG
机构
[1] Aarhus Univ, Marselisborg Hosp, Dept Dermatol, Res Lab B, DK-8000 Aarhus C, Denmark
[2] Univ Tokyo, Dept Mol Prevent Med, Tokyo, Japan
关键词
atopic dermatitis; thymus and activation regulated cytokine; TARC;
D O I
10.1016/S0923-1811(00)00160-2
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
The CC-chemokine TARC is known to be a ligand for the CCR4 receptor which in turn is known to be expressed selectively on the Th-2-subset of lymphocytes. Atopic dermatitis is generally believed to be a Th-2-type disease. and TARC has been shown to be expressed in the skill lesions of a murine model of AD. IL-10 is an interleukine generally known for its ability to inhibit cytokine production, however it has been found to be highly expressed in the skin from AD patients. We show in this report that IL-10 is able to augment the TARC inducing effects of TNF alpha and IFN gamma in HaCaT cells, a property that may be important in the determination of the composition of the cells of the inflammation in the skin of AD patients. In addition, we show that the IL10 agonist IT 9302, a nona-peptide from the carboxylic end of IL-IO, has the same effect on TARC production from HaCaT cells. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:46 / 54
页数:9
相关论文
共 35 条
[1]   Mast cells of psoriatic and atopic dermatitis skin are positive for TNF-α and their degranulation is associated with expression of ICAM-1 in the epidermis [J].
Ackermann, L ;
Harvima, IT .
ARCHIVES OF DERMATOLOGICAL RESEARCH, 1998, 290 (07) :353-359
[2]  
[Anonymous], ACTA DERM VENERE S92, DOI [10.2340/00015555924447, DOI 10.2340/00015555924447]
[3]   IL-10 is a key cytokine in psoriasis -: Proof of principle by IL-10 therapy:: A new therapeutic approach [J].
Asadullah, K ;
Sterry, W ;
Stephanek, K ;
Jasulaitis, D ;
Leupold, M ;
Audring, H ;
Volk, HD ;
Döcke, WD .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (04) :783-794
[4]   Interleukin 10 treatment of psoriasis -: Clinical results of a phase 2 trial [J].
Asadullah, K ;
Döcke, WD ;
Ebeling, M ;
Friedrich, M ;
Belbe, G ;
Audring, H ;
Volk, HD ;
Sterry, W .
ARCHIVES OF DERMATOLOGY, 1999, 135 (02) :187-192
[5]   KERATINOCYTES AS INITIATORS OF INFLAMMATION [J].
BARKER, JNWN ;
MITRA, RS ;
GRIFFITHS, CEM ;
DIXIT, VM ;
NICKOLOFF, BJ .
LANCET, 1991, 337 (8735) :211-214
[6]   DIFFERENT INSITU DISTRIBUTION PATTERNS OF DENDRITIC CELLS HAVING LANGERHANS (T6+) AND INTERDIGITATING (RFD1+) CELL IMMUNOPHENOTYPE IN PSORIASIS, ATOPIC-DERMATITIS, AND OTHER INFLAMMATORY DERMATOSES [J].
BOS, JD ;
VANGARDEREN, ID ;
KRIEG, SR ;
POULTER, LW .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1986, 87 (03) :358-361
[7]  
BOUKAMP P, 1994, KERATINOCYTE HDB, P485
[8]   The chemokine receptor CCR4 in vascular recognition by cutaneous but not intestinal memory T cells [J].
Campbell, JJ ;
Haraldsen, G ;
Pan, J ;
Rottman, J ;
Qin, S ;
Ponath, P ;
Andrew, DP ;
Warnke, R ;
Ruffing, N ;
Kassam, N ;
Wu, L ;
Butcher, EC .
NATURE, 1999, 400 (6746) :776-780
[9]   Localization of monocyte chemotactic and activating factor (MCAF/MCP-1) in psoriasis [J].
Deleuran, M ;
Buhl, L ;
Ellingsen, T ;
Harada, A ;
Larsen, CG ;
Matsushima, K ;
Deleuran, B .
JOURNAL OF DERMATOLOGICAL SCIENCE, 1996, 13 (03) :228-236
[10]  
ENK AH, 1992, J IMMUNOL, V149, P92