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T-cells, as part of the adaptive immune system, have been labelled the main drivers of graft-versus-host disease (GvHD) development. Although current therapeutic strategies for GvHD are largely focused on the modulation of the adaptive immune system, it has become clear that components of the innate immune system are also essential for the progression of GvHD.
The type 2 cannabinoid receptor (CB2R) is a G protein-coupled receptor expressed on almost all immune cells, and controls cytokine release, macrophage-mediated responses, and B- and T-cell differentiation. In humans, genetic perturbances in the CB2R gene have been associated with inflammatory disorders; therefore, targeting CB2R therapeutically is an area of interest in immune-related disease states such as GvHD.
Cheng Yin Yuan and colleagues implemented a pre-clinical study to define the role of CB2R in acute and chronic GvHD (a/cGvHD) development and to determine whether pharmacological modulation of CB2R could alleviate GvHD in murine models. Their results have recently been published in Blood.1
The findings from this study highlight the role of CB2R in immune modulation. A lack of CB2R on donor T cells and pharmacological antagonism of CB2R worsened GvHD and led to the expansion of CD8+ T cells. This indicates that CB2R expression on T cells regulates CD8+ T cell alloreactivity.
The study also uncovered a decline in CB2R expression on T cells, but not macrophages, following aGvHD initiation. This provides information regarding the receptor’s expression patterns in inflammatory conditions.
The CB2R agonists, THC and JWH-133, alleviated T cell-mediated aGvHD and macrophage-driven cGvHD, respectively. The differential disease biology between the two conditions highlight the distinct mechanisms of action of the agonists. The study suggests that effective therapeutic intervention is dependent on the agonist properties in combination with the composition of pathogenic immune cells present in a/cGvHD.
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