Chemokine immune modulation

Immune Modulation by Secreted Chemokine Binding Proteins (CKBPs)... 

At least some of the cannabinoid-induced modulation of immune cells, and effects on host resistance to infection, are mediated directly by binding of cannabinoids to CBRs, particularly CBR2. Host immunity to microbes, however, involves many cell types, both immune and non-immune, as well as soluble factors including cytokines, chemokines, neurocytokines, and hormones related to the HP axis. It is therefore likely that a variety of cellular and molecular mechanisms whereby cannabinoids, including THC, affect immune function. 

Several opiate receptors have been identified on cells of the nervous systems of animals and humans, with mu (p), kappa (k), and gamma (y) subtypes being predominant. These classical opiate receptors are G- protein coupled 7-transmembrane molecules.27 Opiates predominantly affect immune responses directly by ligation of p, k, and y opiate receptors, as well as non-classical opiate-like receptors, on immune cells and indirectly by binding to receptors on CNS cells. Studies conducted in vitro with opiate-treated immune cells demonstrated receptor-mediated reduced phagocytosis, chemotaxis and cytokine and chemokine production. These effects are linked to modulation of host resistance to bacterial, protozoan, viral and fungal infections using animal models, cell lines and primary cells. 

Chemokines have been implicated in diverse pathophysiological functions in allergic inflammation including chemoattraction, cellular activation, hematopoiesis, homeostatic role, and modulation of T cell immune response (R6). 

Trichothecenes inhibit synthesis of protein, RNA and DNA as well as mitochondrial and electron transport chain function stimulate lipid peroxidation alter cell membrane function induce apoptosis modulate immune responses activate mitogen-activated protein kinases (MAPKs) and induce gene expression of numerous chemokines and cytokines and alter neurotransmitter levels. 

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