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Cannabinoid receptors and T helper cells
Thomas W Klein1, Cathy Newton, Kellie Larsen
1Department of Medical Microbiology and Immunology, University of South Florida, 12901 Bruce Downs Boulevard, Tampa, FL 33612, USA. tklein@hsc.usf.edu
Journal of Neuroimmunology
|January 27, 2004
Summary
Delta(9)-tetrahydrocannabinol (THC) from marijuana suppresses T helper 1 cell immunity via CB1 receptors and enhances T helper 2 activity through CB2 receptors, impacting interleukin production.
Area of Science:
- Immunology
- Pharmacology
- Microbiology
Background:
- Delta(9)-tetrahydrocannabinol (THC) administration prior to Legionella pneumophila (Lp) infection in mice suppresses T helper 1 (Th1) cell activity.
- This suppression is associated with reduced interleukin (IL)-12 and interferon (IFN)-gamma, and increased IL-4, indicating a Th1 to Th2 cell bias.
Purpose of the Study:
- To investigate the specific mechanisms of T helper cell biasing induced by THC during Lp infection.
- To determine the roles of cannabinoid receptors CB1 and CB2 in mediating THC's effects on Th1 and Th2 activity.
Main Methods:
- Mice were injected with THC, followed by Lp infection.
- Spleens were analyzed for messenger RNA (mRNA) expression of IL-12Rbeta2 (Th1 marker) and GATA3 (Th2 marker).
- Cannabinoid receptor antagonists (SR1 for CB1, SR2 for CB2) were used to block receptor activity.
Main Results:
- THC suppressed IL-12Rbeta2 mRNA expression but increased GATA3 mRNA expression.
- The CB1 antagonist SR1 attenuated the suppression of IL-12Rbeta2.
- The CB2 antagonist SR2 attenuated the increase in GATA3 mRNA.
Conclusions:
- THC suppresses Th1 biasing activity, indicated by IL-12Rbeta2 levels, through a CB1-mediated mechanism.
- THC enhances Th2 biasing activity, indicated by GATA3 levels, via a CB2-mediated mechanism.
- The differential involvement of CB1 and CB2 receptors suggests distinct roles in regulating Th1 and Th2 cell responses.