Are deficiencies of prostaglandin‐E‐mediated immunoregulation involved in increased IgE synthesis of atopic mononuclear cells in vitro?

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Abstract
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 ω-6-fatty acids.