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Clinical Immunology Section and
Medical Virology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Regulation of the factors governing IL-12R expression and IL-12
responsiveness has been shown to be important in the generation and
stability of Th1- and Th2-type responses. In this regard, cytokines
have been shown to have a prominent role in regulating IL-12R
expression. In this study, the role that PGE2 and
dexamethasone (DXM) have in regulating IL-12R expression was evaluated.
Addition of PGE2 or DXM to human PBMCs stimulated with
immobilized anti-CD3 plus IL-12 inhibited the production of IFN-
in a dose-responsive manner. Moreover, PBMCs stimulated with
immobilized anti-CD3 in the presence of PGE2 or DXM for
3 days, washed extensively, and restimulated in the presence of IL-12
still did not produce IFN-. This lack of IL-12 responsiveness from
cells cultured in either PGE2 or DXM was correlated with
diminished surface expression of IL-12Rß1, IL-12Rß2 mRNA
expression, and IL-12 binding. Finally, the PGE2- and
DXM-mediated inhibition of IL-12R expression was not affected
significantly by addition of neutralizing Abs against either IL-4,
IL-10, or TGF-ß. By contrast, addition of dibutyryl cAMP,
8-bromoadenosine 3:5 cAMP (8-Br-cAMP), or cholera toxin substantially
reduced IL-12R expression, suggesting that PGE2 may be
mediating its effects through enhancement of
cAMP.
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