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 b...

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Bibliographic Details
Published inAllergy (Copenhagen) Vol. 46; no. 7; p. 502
Main Authors Melnik, B, Plewig, G, Tschung, T
Format Journal Article
LanguageEnglish
Published Denmark 01.10.1991
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Summary: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.
ISSN:0105-4538
DOI:10.1111/j.1398-9995.1991.tb00612.x