Abstract
Our hypothesis on the origin of atopy links alterations in omega-6-fatty acid metabolism in atopic persons (i.e., reduced formation of delta-6-desaturase products) to deficient T cell differentiation and function. We suggest that a relative deficiency in dihomo-gamma-linolenic acid-derived prostaglandin E1 is the major etiologic factor for diminished T cell maturation postpartum. Its precursors, gamma-linolenic acid and dihomo-gamma-linolenic acid, are physiologically provided in colostrum and mature breast milk of healthy mothers. Depressed cell-mediated immunity and uncontrolled B-cell response with increased IgE synthesis are explained as prostaglandin E1-dependent defects of T cell differentiation caused by insufficient supply of prostaglandin E1 precursors during early infancy. Thus, in our opinion atopy is a metabolic disorder and the associated immunologic disturbances are epiphenomena.
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