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Published online before print April 24, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0107051

Received for publication January 22, 2007.
Revised March 29, 2007.
Accepted for publication April 1, 2007.

Article

G-protein-coupled receptor expression, function, and signaling in macrophages

Jane Lattin *, David A. Zidar {dagger}, Kate Schroder *, Stuart Kellie *{ddagger}, David A. Hume *{sect}, and Matthew J. Sweet *{ddagger}@

*Cooperative Research Centre for Chronic Inflammatory Diseases and {sect}Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, and {ddagger}School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia; and {dagger}Division of Cardiology, Duke University Medical Center, Durham, North Carolina, USA

@ To whom correspondence should be addressed. E-mail: m.sweet{at}imb.uq.edu.au.


  Abstract

G-protein-coupled receptors (GPCRs) are widely targeted in drug discovery. As macrophages are key cellular mediators of acute and chronic inflammation, we review here the role of GPCRs in regulating macrophage function, with a focus on contribution to disease pathology and potential therapeutic applications. Within this analysis, we highlight novel GPCRs with a macrophage-restricted expression profile, which provide avenues for further exploration. We also review an emerging literature, which documents novel roles for GPCR signaling components in GPCR-independent signaling in macrophages. In particular, we examine the crosstalk between GPCR and TLR signaling pathways and highlight GPCR signaling molecules, which are likely to have uncharacterized functions in this cell lineage.

Key Words: {beta}-arrestin • heterotrimeric • immune • Toll-like receptor • kinase • inflammation




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