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

被引:42
作者
Fedyk, ER
Adawi, A
Looney, RJ
Phipps, RP
机构
[1] UNIV ROCHESTER, SCH MED & DENT, CTR CANC, PROGRAM IMMUNOL, ROCHESTER, NY 14642 USA
[2] UNIV ROCHESTER, SCH MED & DENT, CTR CANC, THORAC ONCOL PROGRAM, ROCHESTER, NY 14642 USA
[3] UNIV ROCHESTER, SCH MED & DENT, DEPT MICROBIOL & IMMUNOL, ROCHESTER, NY 14642 USA
[4] UNIV ROCHESTER, SCH MED & DENT, DEPT MED, ROCHESTER, NY 14642 USA
[5] UNIV ROCHESTER, SCH MED & DENT, DEPT ENVIRONM MED & PEDIAT, ROCHESTER, NY 14642 USA
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1996年 / 81卷 / 02期
关键词
D O I
10.1006/clin.1996.0165
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 beta(2)-adrenergic receptor agonists (beta(2)-agonists), are used to treat asthma. A number of detrimental phenomena have been associated with beta(2)-agonist use such as, rebound hyperresponsiveness and increases in asthma mortality, This review theorizes that beta(2)-agonists enhance IgE and Th2 cytokine production and that these mediators exacerbate extrinsic, IgE-dependent asthma. (C) 1996 Academic Press, Inc.
引用
收藏
页码:101 / 113
页数:13
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