Journal
JOURNAL OF NEUROIMMUNE PHARMACOLOGY
Volume 12, Issue 3, Pages 544-554Publisher
SPRINGER
DOI: 10.1007/s11481-017-9744-7
Keywords
Cannabinoids; Cannabinoid receptor CB2; G protein-coupled receptors; Intracellular membrane receptors; B cells; B cell activation
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Funding
- National Institute on Drug Abuse, National Institutes of Health [5-R01-DA037102]
- Ruth L. Kirschstein National Research Service Award (NRSA) Individual Predoctoral Fellowship to Promote Diversity in Health-Related Research from the National Institute on Drug Abuse, National Institutes of Health [1 F31 DA036293]
- North American Graduate Fellowship Award from the American College of Toxicology
- National Institutes of Health [CA-16042, AI-28697]
- JCCC at UCLA
- UCLA AIDS Institute at UCLA
- David Geffen School of Medicine at UCLA
- NIH-NCRR shared resources grant [CJX1-443835-WS-29646]
- NSF Major Research Instrumentation grant [CHE-0722519]
- National Institutes of Health Award [AI-28697]
- UCLA Council of Bioscience Resources
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Cannabinoid receptor type 2 (CB2) is the primary receptor pathway mediating the immunologic consequences of cannabinoids. We recently reported that human peripheral blood B cells express CB2 on both the extracellular membrane and at intracellular sites, where-as monocytes and T cells only express intracellular CB2. To better understand the pattern of CB2 expression by human B cells, we examined CD20(+) B cells from three tissue sources. Both surface and intracellular expression were present and uniform in cord blood B cells, where all cells exhibited a naive mature phenotype (IgD(+)/ CD38(Dim)). While naive mature and quiescent memory B cells (IgD(-)/CD38(-)) from tonsils and peripheral blood exhibited a similar pattern, tonsillar activated B cells (IgD(-)/CD38(+)) expressed little to no surface CB2. We hypothesized that regulation of the surface CB2 receptor may occur during B cell activation. Consistent with this, a B cell lymphoma cell line known to exhibit an activated phenotype (SUDHL-4) was found to lack cell surface CB2 but express intracellular CB2. Furthermore, in vitro activation of human cord blood resulted in a down-regulation of surface CB2 on those B cells acquiring the activated phenotype but not on those retaining IgD expression. Using a CB2 expressing cell line (293 T/CB2-GFP), confocal microscopy confirmed the presence of both cell surface expression and multifocal intracellular expression, the latter of which co-localized with endoplasmic reticulum but not with mitochondria, lysosomes, or nucleus. Our findings suggest a dynamic multi-compartment expression pattern for CB2 in B cells that is specifically modulated during the course of B cell activation.
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