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Clin Immunol Immunopathol. 1996 Nov;81(2):101-13.

Regulation of IgE and cytokine production by cAMP: implications for extrinsic asthma.

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Immunology Program of the Cancer Center, University of Rochester School of Medicine and Dentistry, New York 14642, USA.


Recent investigations indicate that pharmacologic agents which elevate intracellular levels of cyclic AMP (cAMP) also enhance immunoglobulin E (IgE) production. This review proposes that elevation of intracellular cAMP is a prominent mechanism which enhances IgE production. Enhancement is mediated by two mechanisms. First, cAMP-elevating agents directly target B lymphocytes, promoting recombination of the Ig heavy chain loci. Second, these agents indirectly promote IgE production by inducing a T-helper type 2 (Th2) profile of cytokine secretion. In turn, Th2-type cytokines interact with B lymphocytes and direct isotype switching to the epsilon locus. One type of cAMP-elevating agents, the beta2-adrenergic receptor agonists (beta2-agonists), are used to treat asthma. A number of detrimental phenomena have been associated with beta2-agonist use such as, rebound hyperresponsiveness and increases in asthma mortality. This review theorizes that beta2-agonists enhance IgE and Th2 cytokine production and that these mediators exacerbate extrinsic, IgE-dependent asthma.

[Indexed for MEDLINE]

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