Trillium Therapeutics Inc (TRIL)

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Antibodies could combat atherosclerosis as well as tumor

http://news.xinhuanet.com/english/2016-08/02/c_135556177.htm

In a new study, published recently online in Nature, reserachers at Stanford and two other U.S. universities report that CD47 is extremely abundant in atherosclerotic tissue compared with normal vascular tissue, and correlated with risk for adverse clinical outcomes such as stroke.

Their findings were based on genetic analyses of hundreds of human coronary and carotid artery tissue samples collected at Stanford and at Karolinska Institute in Sweden. And looking at data from other genetic research, they learned that surplus CD47 in atherosclerotic plaques strongly correlates with elevated levels of a well-known inflammation-promoting substance called TNF-alpha.

Further experiments showed that TNF-alpha activity prevents what would otherwise be a progressive decrease of CD47 on dying cells, according to a release from Stanford Medicine News Center. Hence, those cells are less susceptible to being eaten by macrophages.

Atherosclerosis is caused by the deposition of fatty substances along arterial walls. Over the years, these substances form plaques. It is known that numerous dead and dying cells accumulate in plaques, which inflammation renders brittle and vulnerable to rupture, the ultimate cause of heart attack and stroke.

As a cell approaches death, its CD47 surface proteins normally start disappearing, exposing the cell to macrophages' garbage-disposal service. But atherosclerotic plaques are filled with dead and dying cells that should have been cleared by macrophages, yet weren't. In fact, many of the cells piling up in these lesions are dead macrophages and other vascular cells that should have been cleared long ago.

"It seems that heart disease may be driven by our immune system's inability to 'take out the trash,'" Nicholas Leeper, associate professor of vascular surgery and of cardiovascular medicine at Stanford, was quoted as saying.