Immune cells called macrophages, trying to clear the mess, eventually choke and die, worsening the situation.
Dr Chapman's plan was to use this mechanism to get macrophages to eat toxin molecules.
Cells called macrophages summon all sorts of others to an injury, to try to repair it.
These fats can fill macrophages to form small to large nodules under the skin called xanthomas.
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The immune cells, called macrophages, act as little garbage-disposal cells, gobbling up the cholesterol in an attempt to remove it.
Though they may remain in those macrophages for a long time, Dr West says that this longevity does not seem to cause problems.
They found that Salmonella with an inactivated SifA gene no longer has this ability to multiply, and can be killed off by the macrophages.
In the mid-1990s researchers found that when they deleted genes responsible for attracting macrophages to the arteries, atherosclerosis all but disappeared--in lab animals, at least.
The problem is that macrophages have no synaptotagmin on their surfaces.
However, once the macrophages enter the tumour the virus can replicate.
They focused on macrophages, cells which produce proteins called cytokines.
They added resveratrol to the samples and found it reduced the production of a particular cytokine, interleukin 8, by 94% in smokers' macrophages and by 88% in COPD macrophages.
Doctors at the Washington University School of Medicine investigated the role of macrophages, a part of the immune system, in the transition from the dry to the wet form of the disease.
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It is a long way from there to a treatment, but Dr Chapman has made the trick work in mice as well as Petri dishes (injecting the complex does, indeed, stop macrophages recruiting).
One possible cause of their vulnerability is that the virus has evolved around its problem, and found a way to use a slightly different chemokine receptor as a way into its target macrophages.
However, their research showed that older macrophages struggle.
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In 1979 pathologist Ross Gerrity showed that in pigs one of the first steps in the formation of artery plaque occurs when macrophages travel into the artery and gobble up cholesterol inside, forming fatty deposits.
Over the next decade animal studies at UCLA and elsewhere showed that macrophages are attracted to arteries when cholesterol lodged in the arteries gets chemically altered, or oxidized, so that the immune system suddenly spots it as foreign and goes on the attack.
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