The CB2 receptor and its role as a regulator of inflammation.

Caroline Turcotte,Nicolas Flamand,Michel Laviolette,Marie-Renée Blanchet

doi:10.1007/s00018-016-2300-4

Abstract

The CB2 receptor is the peripheral receptor for cannabinoids. It is mainly expressed in immune tissues, highlighting the possibility that the endocannabinoid system has an immunomodulatory role. In this respect, the CB2 receptor was shown to modulate immune cell functions, both in cellulo and in animal models of inflammatory diseases. In this regard, numerous studies have reported that mice lacking the CB2 receptor have an exacerbated inflammatory phenotype. This suggests that therapeutic strategies aiming at modulating CB2 signaling could be promising for the treatment of various inflammatory conditions. Herein, we review the pharmacology of the CB2 receptor, its expression pattern, and the signaling pathways induced by its activation. We next examine the regulation of immune cell functions by the CB2 receptor and the evidence obtained from primary human cells, immortalized cell lines, and animal models of inflammation. Finally, we discuss the possible therapies targeting the CB2 receptor and the questions that remain to be addressed to determine whether this receptor could be a potential target to treat inflammatory disease.

Highlights

The psychotropic effects induced by cannabis promoted its widespread use among the population
We examine the regulation of immune cell functions by the CB2 receptor and the evidence obtained from primary human cells, immortalized cell lines, and animal models of inflammation
It was initially believed that it was not expressed in non-immune cells of the central nervous system, because Munro et al did not detect CB2 receptor mRNA in any brain part when they cloned the receptor [3], which is supported by many studies [40, 54, 58, 59]

Summary

Introduction

The psychotropic effects induced by cannabis promoted its widespread use among the population. The CB2 receptor was shown to modulate immune cell functions, both in cellulo and in animal models of inflammatory diseases. It was initially believed that it was not expressed in non-immune cells of the central nervous system, because Munro et al did not detect CB2 receptor mRNA in any brain part when they cloned the receptor [3], which is supported by many studies [40, 54, 58, 59].

Results

Conclusion