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Cannabinoid receptor activation blocks HIV Tat protein induced macrophage migration: a new avenue for therapeutics

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We all are very familiar with the effects of cannabinoid receptor stimulation on the body. Relaxation, pain relief, and increased appetite probably come first to mind. These psychoactive effects result from activation of the CB1 receptor found on cells in the brain by tetrahydrocannabinol (THC).

But there is another receptor, called CB2, that can bind THC and other natural ligands for the cannabinoid receptor. The CB2 receptor is found on cells comprising the immune system and have a multitude of anti-inflammatory and immunosuppressive effects upon activation. In most cases, immunosuppressive effects are undesirable, but sometimes that can be beneficial. Today’s article is an example.

New research from the lab of Dr. Guy Cabral at Virginia Commonwealth University shows that stimulation of the CB2 receptor on macrophages inhibits migration of healthy immune cells towards the HIV Tat protein. Tat is an essential viral regulatory protein used by HIV to stimulate inflammatory responses and wreak havoc in the body. Tat protein looks suspiciously like some of our own chemokine proteins and can bind to a variety of receptors on immune cells causing activation of cascades that lead to migration of uninfected macrophages towards the HIV infected cells.

The paper by Erinn S. Raborn and Guy A. Cabral, published in the January 2010 issue of the Journal of Pharmacology and Experimental Therapeutics is titled: Cannabinoid Inhibition of Macrophage Migration to the Tat Protein of HIV-1 is Linked to the CB2 Cannabinoid Receptor. The authors used a macrophage cell line in a migration model system to demonstrate very specifically that when the CB2 receptor is stimulated, macrophages no longer respond to the Tat protein. The chemoattractant effects are abolished.

To read a summary of their experiments and exciting results, click the link above.
 
 

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