Leukocytes of patients with atopic eczema exhibit a variety of biochemical abnormalities, particularly an alteration in cyclic nucleotide metabolism. The basic defect is an elevation of phosphodiesterase activity in these cells, which leads to a diminished modulation of cellular immune function by cAMP. This, in turn, leads to an elevation of IgE synthesis and enhanced release of inflammatory mediators from mast cells and basophils. The phosphodiesterase defect offers new approaches to the treatment of atopic eczema.
|Number of pages||4|
|Publication status||Published - 1987|
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