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Δ-Tetrahydrocannabinol Suppresses Cytotoxic T Lymphocyte Function Independent of CB and CB, Disrupting Early Activation Events.
Δ-Tetrahydrocannabinol Suppresses Cytotoxic T Lymphocyte Function Independent of CB and CB, Disrupting Early Activation Events.
- Source :
- Journal of NeuroImmune Pharmacology; Dec2012, Vol. 7 Issue 4, p843-855, 13p, 8 Graphs
- Publication Year :
- 2012
-
Abstract
- Previously, CD8 T cells were found to be a sensitive target for suppression by Δ-tetrahydrocannabinol (Δ-THC) in a murine model of influenza infection. To study the effect of Δ-THC on CD8 cytotoxic T lymphocytes (CTL), an allogeneic model of MHC I mismatch was used to elicit CTL. In addition, to determine the requirement for the cannabinoid receptors 1 (CB) and 2 (CB) in Δ-THC-mediated CTL response modulation, mice null for both receptors were used (CBCB). Δ-THC suppressed CTL function independent of CB and CB as evidenced by reduction of Cr release by CTL generated from CBCB mice. Furthermore, viability in CD4 and CD8 cells was reduced in a concentration-dependent manner with Δ-THC, independent of CB and CB, but no effect of Δ-THC on proliferation was observed, suggesting that Δ-THC decreases the number of T cells initially activated. Δ-THC increased expression of the activation markers, CD69 in CD8 cells and CD25 in CD4 cells in a concentration-dependent manner in cells derived from WT and CBCB mice. Furthermore, Δ-THC synergized with the calcium ionophore, ionomycin, to increase CD69 expression on both CD4 and CD8 cells. In addition, without stimulation, Δ-THC increased CD69 expression in CD8 cells from CBCB and WT mice. Overall, these results suggest that CB and CB are dispensable for Δ-THC-mediated suppression and that perturbation of Ca signals during T cell activation plays an important role in the mechanism by which Δ-THC suppresses CTL function. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 15571890
- Volume :
- 7
- Issue :
- 4
- Database :
- Complementary Index
- Journal :
- Journal of NeuroImmune Pharmacology
- Publication Type :
- Academic Journal
- Accession number :
- 83879562
- Full Text :
- https://doi.org/10.1007/s11481-011-9293-4