Author: ["Katarzyna Maresz","Gareth Pryce","Eugene D Ponomarev","Giovanni Marsicano","J Ludovic Croxford","Leah P Shriver","Catherine Ledent","Xiaodong Cheng","Erica J Carrier","Monica K Mann","Gavin Giovannoni","Roger G Pertwee","Takashi Yamamura","Nancy E Buckley","Cecilia J Hillard","Beat Lutz","David Baker","Bonnie N Dittel"]
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Abstract
The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB1 and CB2 cannabinoid receptors in regulating CNS autoimmunity. We found that CB1 receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB2 receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB2-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher rate of proliferation and increased production of inflammatory cytokines, resulting in severe clinical disease. Together, our results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.Cite this article
Maresz, K., Pryce, G., Ponomarev, E. et al. Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells. Nat Med 13, 492–497 (2007). https://doi.org/10.1038/nm1561 