Phosphodiesterase and immune dysfunction in atopic dermatitis

Jon M. Hanifin

Research output: Contribution to journalReview articlepeer-review

21 Scopus citations


Atopic dermatitis and the other atopic conditions occur as a result of direct or indirect influences from cells of hematopoietic origin. Cellular immune abnormalities have been described, but appear to be secondary to cutaneous inflammation in atopic dermatitis. Pharmacophysiologic abnormalities are numerous and may relate to defective cyclic nucleotide metabolism in circulating and infiltrating leukocytes. A consistent leukocyte abnormality is elevated cyclic AMP-phosphodiesterase. This enzyme abnormality results in reduced intracellular cyclic AMP, creating a net permissive effect upon cell function. Phosphodiesterase inhibitors have been demonstrated to reduce abnormal histamine release and IgE production by cultured leukocytes. Studies of phosphodiesterase and associated defects in atopic leukocytes may lead to delineation of basic pathogenetic mechanisms as well as providing the potential for therapeutic targeting.

Original languageEnglish (US)
Pages (from-to)1-6
Number of pages6
JournalJournal of Dermatological Science
Issue number1
StatePublished - Jan 1990


  • Atopic dermatitis
  • Atopic leukocytes
  • Immune dysfunction
  • Pathogenic mechanisms
  • Phosphodiesterase
  • Therapeutic targeting

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology


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