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Regulation of G-protein-coupled signaling pathways in allergic inflammation

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Abstract

Allergic diseases such as asthma are elicited by maladaptive activation of immune cells such as mast cells and lymphocytes by otherwise innocuous allergens. The numerous mediators secreted by such cells promote both acute inflammation and, in many instances, chronic tissue remodeling. Most of these compounds exert their effects on end-organ targets such as epithelial and endothelial cells and airway smooth muscle by activating G-protein-coupled receptors (GPCRs), which are by far the most abundant type of cell surface receptor. Since GPCRs are also the most common target of allergy therapeutics, a better understanding of their intracellular signaling mechanisms is vital to improve the efficacy of such drugs or to develop new targets. In this review, we focus on some of the new regulatory elements that control the duration and amplitude of GPCR signal transduction pathways in immune effector cells and end-organ structural cells affected by allergic inflammation.

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Acknowledgments

The author thanks Dr. Zhihui Xie, our generous collaborators, and members of the Laboratory of Allergic Diseases for invaluable input and discussion. This work was supported by the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.

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Correspondence to Kirk M. Druey.

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Druey, K.M. Regulation of G-protein-coupled signaling pathways in allergic inflammation. Immunol Res 43, 62–76 (2009). https://doi.org/10.1007/s12026-008-8050-0

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