PROSTAGLANDIN E(2) CONTROL OF T-CELL CYTOKINE PRODUCTION IS FUNCTIONALLY RELATED TO THE REDUCED LYMPHOCYTE-PROLIFERATION IN ATOPIC-DERMATITIS

Citation
S. Chan et al., PROSTAGLANDIN E(2) CONTROL OF T-CELL CYTOKINE PRODUCTION IS FUNCTIONALLY RELATED TO THE REDUCED LYMPHOCYTE-PROLIFERATION IN ATOPIC-DERMATITIS, Journal of allergy and clinical immunology, 97(1), 1996, pp. 85-94
Citations number
27
Categorie Soggetti
Immunology,Allergy
ISSN journal
00916749
Volume
97
Issue
1
Year of publication
1996
Part
1
Pages
85 - 94
Database
ISI
SICI code
0091-6749(1996)97:1<85:PECOTC>2.0.ZU;2-O
Abstract
Past studies of peripheral blood mononuclear cells (PBMC) from patient s with atopic dermatitis (AD) have demonstrated reduced proliferation. We have studied phytohemagglutinin-induced lymphocyte proliferation i n the context of interleukin-4 (IL-4), interferon-gamma (IFN-gamma), a nd prostaglandin E(2) (PGE(2)) production in cultures of PBMC from pat ients without and with AD. The production index was found to correlate proportionally to IFN-gamma production and inversely to T-cell IL-4 a nd monocyte PGE(2) production. Assays in parallel cultures showed sign ificantly increased PGE(2) production by purified AD monocytes. The pr oliferation index in PBMC from persons with AD was significantly reduc ed compared with normal PBMC. This difference was normalized in the pr esence of extrinsic IFN-gamma but exaggerated when IL-4 was added. Inc reased AD monocyte production of inflammatory factors (e.g., PGE(2)) a nd cytokines appears to increase IL-4 production by Th2 while suppress ing IFN-gamma by Tk1. Restoration of the normal proliferation of PBMC by the addition of IFN-gamma may represent one mechanism for the clini cal efficacy of IFN-gamma treatment of AD.