Abstract
The cannabinoid CB2 receptor was cloned from the promyeloid cell line HL-60 and is notably expressed in most, if not all leukocyte types. This relatively restricted localization, combined to the absence of psychotropic effects following its activation, make it an attractive drug target for inflammatory and autoimmune diseases. Therefore, there has been an increasing interest in the past decades to identify precisely which immune cells express the CB2 receptor and what are the consequences of such activation. Herein, we provide new data on the expression of both CB1 and CB2 receptors by human blood leukocytes and discuss the impact of CB2 receptor activation in human leukocytes. While the expression of the CB2 mRNA can be detected in eosinophils, neutrophils, monocytes, B and T lymphocytes, this receptor is most abundant in human eosinophils and B lymphocytes. We also review the evidence obtained from primary human leukocytes and immortalized cell lines regarding the regulation of their functions by the CB2 receptor, which underscore the urgent need to deepen our understanding of the CB2 receptor as an immunoregulator in humans.
Highlights
The cannabinoid receptors 1 and 2 (CB1 and CB2) are two G protein-coupled receptors that function through binding a vast array of ligands including phytocannabinoids and endocannabinoids (Di Marzo et al, 1998; Turcotte et al, 2015)
The CB1 receptor, highly expressed in the brain, was the first cannabinoid receptor identified through its responsiveness to Δ9-tetrahydrocannabinol (Δ9-THC) and cloned (Devane et al, 1988; Matsuda et al, 1990)
The CB2 receptor was later cloned from HL-60 cells and identified on its 44% aminoacid homology with the CB1, as well as its similar binding profile to the endocannabinoid N-arachidonoylethanolamine (AEA) and Δ9-THC (Munro et al, 1993)
Summary
The cannabinoid receptors 1 and 2 (CB1 and CB2) are two G protein-coupled receptors that function through binding a vast array of ligands including phytocannabinoids and endocannabinoids (Di Marzo et al, 1998; Turcotte et al, 2015). While some documented the expression of the CB2 receptor in human granulocytes (neutrophils and contaminating eosinophils) (Galiegue et al, 1995; Kurihara et al, 2006), others did not (Oka et al, 2004; Graham et al, 2010) This raised the possibility that contaminating cells might have been responsible for the previously documented CB2 signal in neutrophils, and possibly other cell types. While we detected the expression of the CB2 receptor mRNA in all leukocyte and hypothalamus samples, human eosinophils and B lymphocytes displayed the strongest signals (Figure 1B). These cell types are likely the origin of CB2 expression found in mixed populations such as granulocytes (neutrophils and eosinophils, often abbreviated as PMN) and PBMCs (monocytes, B and T lymphocytes). Activation of the CB2 receptor has been associated with B lymphocyte differentiation, migration, proliferation and antibody class switching (Jorda et al, 2002; Tanikawa et al, 2007; Agudelo et al, 2008), suggesting the receptor is part of the B lymphocytes immune programing,
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