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Protective mechanism discovered against atherosclerosis

last modified Jun 13, 2018 02:52 PM

Dr Dimitrios Tsiantoulas, Dr Andrew Sage, Prof Ziad Mallat, and collaborators led by Prof Christoph Binder at CeMM and the Medical University of Vienna have shown that immune cells promoting inflammation play a critical role in the development of atherosclerosis.

Atherosclerosis, the pathological narrowing of blood vessels, is the underlying cause for the majority of strokes and heart attacks, the major causes of mortality worldwide according to the WHO. For the development of atherosclerosis, a special type of white blood cells called B2 lymphocytes have been suggested to play a crucial role. For their survival, they need a molecule called BAFF. It has been shown previously that inactivation of BAFF receptors at the surface of B2 lymphocytes reduces the development of atherosclerosis in mice. 

BAFF can be bound and neutralized with antibodies. BAFF-specific antibodies where tested for their effects on the development of atherosclerosis in mice and the results were surprising: instead of reducing atherosclerotic lesion formation in the arteries of the tested mice, the antibody treatment led to an increased plaque size.

The researchers found BAFF to have anti-inflammatory properties, which has a positive effect on both plaque size and atherosclerosis risk. The newly discovered mechanism is triggered by an alternative BAFF receptor on the surface of other immune cells called macrophages. It was shown that these cells induce an anti-inflammatory process.

This study, published in Circulation, provides valuable new insight for atherosclerosis research and suggests a hitherto unknown, inherited risk factor for atherosclerosis.

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