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β2-Adrenergic receptors in immunity and inflammation: Stressing NF-κB
被引:101
作者:
Kolmus, Krzysztof
Tavernier, Jan
Gerlo, Sarah
[1
]
机构:
[1] Univ Ghent VIB, Dept Med Prot Res, B-9000 Ghent, Belgium
关键词:
NF-kappa B;
beta(2)-Adrenergic receptor;
Stress;
Inflammation;
Immunomodulation;
Signalling;
NUCLEAR-FACTOR;
PROTEIN-KINASE;
TRANSCRIPTIONAL ACTIVITY;
STRUCTURAL INSIGHTS;
PSYCHOSOCIAL STRESS;
IL-6;
EXPRESSION;
GENE-EXPRESSION;
BETA-BLOCKER;
NITRIC-OXIDE;
LIGAND BIAS;
D O I:
10.1016/j.bbi.2014.10.007
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
beta(2)-Adrenergic receptors (beta(2)-ARs) transduce the effects of (nor)epinephrine on a variety of cell types and act as key mediators of the body's reaction to stress. beta(2)-ARs are also expressed on immune cells and there is ample evidence for their role in immunomodulation. A key regulator of the immune response and a target for regulation by stress-induced signals is the transcription factor Nuclear Factor-kappaB (NF-kappa B). NF-kappa B shapes the course of both innate and adaptive immune responses and plays an important role in susceptibility to disease. In this review, we summarise the literature that has been accumulated in the past 20 years on adrenergic modulation of NF-kappa B function. We here focus on the molecular basis of the reported interactions and show that both physiological and pharmacological triggers of beta(2)-ARs intersect with the NF-kappa B signalling cascade at different levels. Importantly, the action of beta(2)-AR-derived signals on NF-kappa B activity appears to be highly cell type specific and gene selective, providing opportunities for the development of selective NF-kappa B modulators. (C) 2014 Elsevier Inc. All rights reserved.
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页码:297 / 310
页数:14
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