- A protective mechanism against atherosclerosis has been discovered.
- The molecule B cell activating factor (BAFF) plays an important role in the development of atherosclerosis.
- Deletion or blockade of the BAFF receptors reduces the development of atherosclerosis.
A potential target for future atherosclerosis treatments has been identified by a research team at the CEMM Research Center for Molecular Medicine of the Austrian Academy of Sciences.
The research team finds that deletion or blockade of the molecule BAFF receptors at the surface of B2 lymphocytes reduces the development of atherosclerosis
in mice. BAFF is needed for the survival of a type of white blood cells called B2 lymphocytes which play an important role in the development of atherosclerosis.
‘It has been discovered that the molecule BAFF plays an important role in plaque size and atherosclerosis risk and that bloakage of BAFF reduces the development of atherosclerosis.’
With highly specific antibodies, BAFF can be bound and neutralized. Those antibodies where tested for their effects on the development of atherosclerosis in mice by scientists from CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and the Medical University of Vienna in collaboration with the University of Cambridge. The results were surprising: instead of reducing atherosclerotic lesion formation in the arteries of the tested mice, the antibody treatment lead to an increased plaque size.
"We were able to show that B2 lymphocytes were efficiently depleted upon anti-BAFF antibody treatment", senior author of the study Christoph Binder, CeMM Principal Investigator and Professor for Atherosclerosis Research at the Medical University of Vienna, describes the results of the study. "Surprisingly, the plaque size increased, indicating a hitherto unknown role of the BAFF molecule in atherosclerosis. However, in further experiments, we were able to explain these findings."
The researchers found BAFF to have anti-inflammatory properties, which has a positive effect on plaque size and atherosclerosis risk. The newly discovered mechanism is triggered by an alternative BAFF receptor - Transmembrane activator and CAML interactor (TACI) on the surface of macrophages, another type of immune cells. It was shown that these cells induce an anti-inflammatory process. This finding may provide important implications for atherosclerosis research and prevention: For example, mutations in the gene for TACI may confer an increased cardiovascular risk.
- BAFF Neutralization Aggravates Atherosclerosis - ( http://circ.ahajournals.org/content/early/2018/05/31/CIRCULATIONAHA.117.032790)