Is the origin of atopy linked to deficient conversion of ω-6-fatty acids to prostaglandin E1?

摘要: Our hypothesis on the origin of atopy links alterations in ω-6-fatty acid metabolism atopic persons (i.e., reduced formation δ-6-desaturase products) to deficient T cell differentiation and function. We suggest that a relative deficiency dihomo-γ-hnolenic acid-derived prostaglandin E 1 is major etiologic factor for diminished maturation postpartum. Its precursors, γ-linolenic dihomo-γ-linolenic acid, are physiologically provided colostrum mature breast milk healthy mothers. Depressed cell-mediated immunity uncontrolled B-cell response with increased IgE synthesis explained as -dependent defects caused by insufficient supply precursors during early infancy. Thus, our opinion metabolic disorder associated immunologic disturbances epiphenomena.