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

Citation
C. Vestergaard et al., IL-10 augments the IFN-gamma and TNF-alpha induced TARC production in HaCaT cells: a possible mechanism in the inflammatory reaction of atopic dermatitis, J DERMA SCI, 26(1), 2001, pp. 46-54
Citations number
35
Categorie Soggetti
Dermatology
Journal title
JOURNAL OF DERMATOLOGICAL SCIENCE
ISSN journal
09231811 → ACNP
Volume
26
Issue
1
Year of publication
2001
Pages
46 - 54
Database
ISI
SICI code
0923-1811(200105)26:1<46:IATIAT>2.0.ZU;2-V
Abstract
The CC-chemokine TARC is known to be a ligand for the CCR4 receptor which i n turn is known to be expressed selectively on the Th-2-subset of lymphocyt es. 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 th e skin from AD patients. We show in this report that IL-10 is able to augme nt the TARC inducing effects of TNF alpha and IFN gamma in HaCaT cells, a p roperty that may be important in the determination of the composition of th e cells of the inflammation in the skin of AD patients. In addition, we sho w 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 El sevier Science Ireland Ltd. All rights reserved.