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* Department of Neuroscience, and
Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
Cannabinoids affect diverse biological processes, including functions of the immune system. With respect to the immune system, anti-inflammatory and immunosuppressive effects of cannabinoids have been reported. Cannabinoids stimulate G protein-coupled cannabinoid receptors CB1 and CB2. These receptors are found primarily on neurons. However, they are also found on dendritic cells (DC), which are recognized for their critical role in initiating and maintaining immune responses. Therefore, DC are potential targets for cannabinoids. We report in this study that cannabinoids reduced the DC surface expression of MHC class II molecules as well as their capacity to stimulate T cells. In the nervous system, CB1 receptor signaling modulates K+ and Ca2+ channels. Interestingly, cannabinoid-treated DC also showed altered voltage-gated potassium (KV) channel function. We speculate that attenuation of KV channel function via CB1 receptor signaling in DC may represent one mechanism by which cannabinoids alter DC function.
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1 This work is supported by grants from the Swedish Research Council, the Swedish Foundation for Strategic Research, and the Karolinska Institutet. This work was also supported by Grants 4480 from the Swedish Research Council and FP-6-19090 from European Commission.
2 Address correspondence and reprint requests to Dr. Mattias Svensson, Center for Infectious Medicine, F59, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Huddinge, 141 86 Stockholm, Sweden. E-mail address: mattias.svensson{at}ki.se
3 Abbreviations used in this paper: KV, voltage-gated potassium; DC, dendritic cell; MHC-II, MHC class II; TEA, tetraethyl-ammonium; ACPA, arachidonylcyclopropylamide; PTX, pertussis toxin.
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