[Frontiers in Bioscience S2, 969-979, June 1, 2010]

Regulation of T cells in airway disease by beta-agonist

Matthew J. Loza, Raymond B. Penn

Department of Medicine, Division of Pulmonary & Critical Care Medicine University of Maryland School of Medicine, Baltimore MD 21201

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. At the cellular/molecular level: T cell signaling
3.1. Antigen-dependent signaling
3.2. Antigen-independent signaling
3.3. Beta-agonist regulation of T cell signaling
4. Asthma, inflammation, and T cells
5. Effects of beta-agonists on T cells
5.1. Effects of beta-agonists in in vivo models of allergic lung inflammation
5.2. Effects of beta-agonists on T cells using cell culture models
6. What's next: futures studies examining beta-agonist effects on T cells
6.1. The fundamental question of the relevance of beta-agonist regulation of T cells
6.2. Agonism properties of various beta-agonists
6.3. Compartmentalization of Beta2AR signaling in T cells
7. Acknowledgement
8. References

1. ABSTRACT

It is widely recognized that Th2 cytokines derived from T cells play a major role in the development of allergic lung inflammation that causes most asthma. Beta-agonists are important rescue and maintenance therapies for asthma, yet our understanding of beta-agonist effects on T cell biology is surprisingly poor. Recent studies using both cell culture and more integrative models are beginning to reveal beta-agonist regulation of T cell signaling and function that may be important in the pathogenesis and treatment of asthma and possibly other inflammatory diseases. Here we provide a comprehensive review of the literature concerning beta-agonist effects on T cells, and discuss the relevance of emerging paradigms of beta-adrenergic receptor signaling to T cell function.