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Study Shows New Cause of Inflammation in Arteriosclerosis

Heart Health Heart Health
Phase 2

Medical researchers are constantly seeking to unveil the “hows” and “whys” of disease states, especially in specific instances.

Some individuals lack specific antibodies—immunoglobulin M (IgM), typically produced following a blood infection, and which kick off the immune response to fight infection. Researchers from both the CeMM (the Austrian Academy of Sciences Research Center for Molecular Medicine), and MedUni Vienna’s Division of Medical-Chemical Laboratory Diagnostics recently discovered how deficiency of IgM can spur an increased risk of arteriosclerosis, that may lead to serious cardiovascular diseases.

According to a press release announcing the study results, IgMs have another role—they maintain an important balance by controlling the development of B cells, which are responsible for producing and disposing of antibodies. They also regulate the blood concentration of immunoglobulin E (IgE) antibodies to ensure balance—which cannot occur in individuals who lack IgM antibodies. The uncontrolled IgE antibodies, which also play a significant role in the development of allergic reactions, lead to the increased formation of plaques, and activation of mast cells and inflammatory processes as well as constrict and damage blood vessels—as shown in the new animal-model study.

“For the first time, we were able to show that IgE antibodies can themselves provoke inflammatory reactions in vessels and that inhibition of these IgE antibodies prevents damage to the vessels,” said Christoph J. Binder, study co-author. Lead author Dimitrios Tsiantoulas added, “We were able to identify a completely new function of IgM antibodies, which also probably plays a major role in the development of allergies.”

Insufficient levels of IgM antibody are found in up to 2.5 percent of the total population, the authors noted.

Tsiantoulas D., et al. “Increased Plasma IgE Accelerate Atherosclerosis in Secreted IgM Deficiency.” Circ Res. 2017;120:00-00. DOI: 10.1161/CIRCRESAHA.116.309606.


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