Are deficiencies of prostaglandin-E-mediated immunoregulation involved in increased IgE synthesis of atopic mononuclear cells in vitro?
We demonstrate that spontaneous in vitro immunoglobulin E synthesis of atopic peripheral blood mononuclear cells could be suppressed by the addition of 10(-6) M to 10(-5) M prostaglandin E1 (PGE1) or PGE2. Impaired suppressor T lymphocyte maturation and function in atopic individuals are explained by an insufficient transmission of prostaglandin E (PGE) signals during thymic lymphocyte differentiation as well as an impaired ability of the atopic immune system to activate suppressor T cells by PGE-mediated feed back mechanisms. Decreased levels of 6-desaturated PGE-precursor fatty acids in plasma, T lymphocytes, monocytes, adipose tissue and breast milk have been observed in atopic individuals. These insights might offer a novel approach to the prevention of atopic disease by substitution of the atopic pregnant and nursing woman and her newborn infant with long-chain omega-6-fatty acids.
Melnik
B
B
Department of Dermatology, Heinrich-Heine-University of Düsseldorf, Germany.
Plewig
G
G
Tschung
T
T
D002478:Cells, Cultured; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000517:prevention & control; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000096:biosynthesis*; D009000:Monocytes / Q000276:immunology*; D011247:Pregnancy; D011458:Prostaglandins E / Q000172:deficiency* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D011458:Prostaglandins E; D007073:Immunoglobulin E