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Researchers discover new way to block inflammation
Date:7/1/2013

d amyloid damage the macrophage and trigger a powerful cytokine, called interleukin-1B, linked to a chronic inflammatory response."

These findings hold exciting clinical implications. When the researchers blocked the CD36 receptor in mice with atherosclerosis (in which cholesterol thickens the arteries), the cytokine response declined, fewer cholesterol crystals formed in plaques, and inflammation decreased. Consequently, atherosclerosis also abated.

Other less-targeted strategies to control inflammation may hamper the immune response, but the CD36 strategy spares certain cytokines to fight off pathogens, while blocking CD36's ability to trigger interleukin-1B.

"Our findings identify CD36 as a central regulator of the immune response in these conditions and suggest that blocking CD36 might be a common therapeutic option for all three diseases," says Dr. Moore.


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Contact: Allison Clair
allison.clair@nyumc.org
212-404-3753
NYU Langone Medical Center / New York University School of Medicine
Source:Eurekalert

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