Cannabinoids Affect Dendritic Cell (DC) Potassium Channel Function and Modulate DC T Cell Stimulatory Capacity
Author(s) -
Paul W. Wacnik,
Katarina M. Luhr,
Russell H. Hill,
HansGustaf Ljunggren,
Krister Kristensson,
Mattias Svensson
Publication year - 2008
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.181.5.3057
Subject(s) - cannabinoid receptor , cannabinoid , microbiology and biotechnology , immune system , receptor , cannabinoid receptor type 2 , dendritic cell , potassium channel , chemistry , biology , neuroscience , biophysics , immunology , biochemistry , agonist
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 Ca(2+) channels. Interestingly, cannabinoid-treated DC also showed altered voltage-gated potassium (K(V)) channel function. We speculate that attenuation of K(V) channel function via CB1 receptor signaling in DC may represent one mechanism by which cannabinoids alter DC function.
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