BAFF neutralization aggravates atherosclerosis

July 16, 2018 0 By CH Unnikrishnan

Dimitrios Tsiantoulas et al have found that anti- B cell activating factor (BAFF) antibody treatment increased atherosclerosis in mice, despite efficient depletion of mature B-2 cells. Genomic data showed that the BAFF receptor pathway is a key driver of coronary heart disease. Deletion or antibody-mediated blockade of BAFFR ablates B-2 cells and decreases experimental atherosclerosis. Immunotherapy against BAFF is approved for treatment of autoimmune systemic lupus erythematosus and can therefore be expected to limit their associated cardiovascular risk.

The researchers treated Apoe and Ldlr mice with a well-characterized blocking anti-BAFF antibody to study the effect of BAFF neutralization in atherosclerosis. To understand the mechanism by which BAFF impacts atherosclerosis, atherosclerosis-prone mice that lack the alternative receptor for BAFF, transmembrane activator and CAML interactor (TACI) were studied.

However, direct effects of anti-BAFF immunotherapy on atherosclerosis remain unknown.