Activation of cannabinoid receptor 2 attenuates synovitis and joint distruction in collagen-induced arthritis

Activation of cannabinoid receptor 2 attenuates synovitis and joint distruction in... Introduction</h5> Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease of unknown etiology, which is characterized by chronic inflammatory infiltration of the synovium, leading to eventual cartilage and bone destruction ( Scott et al. 2010 ). In spite of significant improvements in the treatment of RA, there is still a need for the identification of new pathways involved in the modulation of inflammation in order to further increase efficacy, particularly in patients in whom the disease does not respond to current therapies.</P>Recently, the discovery of endocannabinoid system, especially two subtypes of cannabinoid receptors, has raised a great deal of interest in inflammatory diseases, including multiple sclerosis and RA ( Klein 2005 ). Two accredited types of cannabinoid receptors, cannabinoid receptor 1 (CB1R) and cannabinoid receptor 2 (CB2R), were discovered in the early 1990s ( Matsuda et al. 1990; Munro et al. 1993 ). CB1R exists primarily on central and peripheral neurons, and is associated with the psychoactive effects of cannabinoids. CB2R is predominantly expressed by cells of hematopoietic origin and is thought to mediate cannabinoid-induced immune modulation ( Howlett et al. 2002 ). The level of their expression is dependent on the activation state of the cell and the http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Immunobiology Elsevier

Activation of cannabinoid receptor 2 attenuates synovitis and joint distruction in collagen-induced arthritis

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Publisher
Elsevier
Copyright
Copyright © 2014 Elsevier GmbH
ISSN
0171-2985
eISSN
1878-3279
D.O.I.
10.1016/j.imbio.2014.12.012
Publisher site
See Article on Publisher Site

Abstract

Introduction</h5> Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease of unknown etiology, which is characterized by chronic inflammatory infiltration of the synovium, leading to eventual cartilage and bone destruction ( Scott et al. 2010 ). In spite of significant improvements in the treatment of RA, there is still a need for the identification of new pathways involved in the modulation of inflammation in order to further increase efficacy, particularly in patients in whom the disease does not respond to current therapies.</P>Recently, the discovery of endocannabinoid system, especially two subtypes of cannabinoid receptors, has raised a great deal of interest in inflammatory diseases, including multiple sclerosis and RA ( Klein 2005 ). Two accredited types of cannabinoid receptors, cannabinoid receptor 1 (CB1R) and cannabinoid receptor 2 (CB2R), were discovered in the early 1990s ( Matsuda et al. 1990; Munro et al. 1993 ). CB1R exists primarily on central and peripheral neurons, and is associated with the psychoactive effects of cannabinoids. CB2R is predominantly expressed by cells of hematopoietic origin and is thought to mediate cannabinoid-induced immune modulation ( Howlett et al. 2002 ). The level of their expression is dependent on the activation state of the cell and the

Journal

ImmunobiologyElsevier

Published: Jun 1, 2015

References

  • Cannabinoid receptor 2 counteracts interleukin-17-induced immune and fibrogenic responses in mouse liver
    Guillot, A.; Hamdaoui, N.; Bizy, A.
  • Selective CB2 receptor activation ameliorates EAE by reducing Th17 differentiation and immune cell accumulation in the CNS
    Kong, W.; Li, H.; Tuma, R.F.; Ganea, D.
  • Differential expression of cannabinoid CB(2) receptor mRNA in mouse immune cell subpopulations and following B cell stimulation
    Lee, S.F.; Newton, C.; Widen, R.; Friedman, H.; Klein, T.W.
  • Activation of cannabinoid receptor 2 reduces inflammation in acute experimental pancreatitis via intra-acinar activation of p38 and MK2-dependent mechanisms
    Michler, T.; Storr, M.; Kramer, J.
  • Dimethylheptyl-THC-11 oic acid: a nonpsychoactive antiinflammatory agent with a cannabinoid template structure
    Zurier, R.B.; Rossetti, R.G.; Lane, J.H.; Goldberg, J.M.; Hunter, S.A.; Burstein, S.H.

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