Monocyte phosphodiesterase abnormalities and dysregulation of lymphocyte function in atopic dermatitis

J. M. Hanifin, S. C. Chan

Research output: Contribution to journalArticlepeer-review

93 Scopus citations


The immunologic aberrations associated with atopic dermatitis include the paradox of reduced cell-mediated immune responses in the setting of increased cell-mediated immunity features that resemble allergic contact dermatitis. In this review, we present evidence that abnormalities in monocytes and Langerhans cells alter the function of T-helper-cell sub-populations to cause the immunologic defects associated with atopic dermatitis. Increased monocyte prostaglandin E2 production inhibits Th1 responses, accentuating interleukin (IL)-4 secretion by Th2 cells. Elevated prostaglandin E2 secretion correlates with abnormally increased cyclic adenosine monophosphate-phosphodiesterase activity in monocytes and this, along with other defective inflammatory cell responses, can be normalized in vitro by phosphodiesterase inhibitors. It appears that in addition to prostaglandin E2 IL-10 acts to regulate the balance between Th1 and Th2 functional responses accounting for many atopic features, including increased IL-4, IL-5, and IL-6 production by T cells; increased IgE synthesis; decreased interferon-γ production; and impaired cell-mediated immune responses. All of these abnormalities can be related to increased phosphodiesterase activity in atopic monocytes, and inhibition of this key enzyme appears to reverse atopic dermatitis inflammatory abnormalities in vitro and in vivo.

Original languageEnglish (US)
Pages (from-to)S84-S88
JournalJournal of Investigative Dermatology
Issue number1 SUPPL.
StatePublished - 1995
Externally publishedYes


  • Cell-mediated immunity
  • Interferon-γ
  • Langerhans cells
  • Mononuclear leukocytes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology


Dive into the research topics of 'Monocyte phosphodiesterase abnormalities and dysregulation of lymphocyte function in atopic dermatitis'. Together they form a unique fingerprint.

Cite this