Journal of Neuroimmunology, Vol. 133 (1-2) (2002) pp. 124-131
Michael Yuan a, Sylvia M. Kiertscher a,b, Qingwen Cheng a, Richard Zoumalan a, Donald P. Tashkin a and Michael D. Roth a,b
a Division of Pulmonary and Critical Care Medicine, UCLA School of Medicine, Los Angeles, CA 90095-1690, USA
b Jonsson Comprehensive Cancer Center, UCLA School of Medicine, Los Angeles, CA 90095-1690, USA
Human leukocytes express cannabinoid (CB) receptors, suggesting a role for both endogenous ligands and D9-tetrahydrocannabinol (THC) as immune modulators.
To evaluate this, human T cells were stimulated with allogeneic dendritic cells (DC) in the presence or absence of THC (0.625-5 µg/ml).
THC suppressed T cell proliferation, inhibited the production of interferon-g and shifted the balance of T helper 1 (Th1)/T helper 2 (Th2) cytokines.
Intracellular cytokine staining demonstrated that THC reduced both the percentage and mean fluorescence intensity of activated T cells capable of producing interferon-g, with variable effects on the number of T cells capable of producing interleukin-4.
Exposure to THC also decreased steady-state levels of mRNA encoding for Th1 cytokines, while increasing mRNA levels for Th2 cytokines.
The CB2 receptor antagonist, SR144528, abrogated the majority of these effects.
We conclude that cannabinoids have the potential to regulate the activation and balance of human Th1/Th2 cells by a CB2 receptor-dependent pathway.
© Copyright 2002, Elsevier Science