Cells magnified image
Dendritic cells (illustrated above) derive their name from "dendron," the Greek word for tree, because of the distinctive branching projections on the cells’ surface. (Photo: iStock)

'Tis the season for coughing, sneezing and runny noses. Winter is the time of year when Canadians are most susceptible to the common cold, which is caused by viruses that infect the nose and throat.

Cold viruses are typically harmless and removed by the immune system within a week or two. However, in some people, they can persist and cause problematic infections in other organs.

Cold viruses, along with other several other viruses, can infect the heart causing a condition known as myocarditis. This condition is characterized by inflammation of, and damage to, the heart muscle, compromising its ability to pump blood.

In some cases, the damage is so severe that it leads to heart failure, which occurs when the heart can no longer pump enough blood to meet the body's needs.
Not much is known about viral myocarditis, the immune response in the heart or the mechanisms underpinning the transition from infection to heart failure. These knowledge gaps have precluded the development of specific and more effective treatments for viral myocarditis.

To address this, TGHRI Scientist Dr. Slava Epelman led a study examining dendritic cells (DCs), a type of immune cell, in the heart and their role in viral myocarditis. DCs reside in a variety of other organs, such as the lungs, liver and kidneys, where they initiate the immune response to eliminate disease-causing viruses.

Dr. Epelman and his colleagues discovered that the heart contains at least five different kinds of DCs, the two most abundant of which are referred to as CD103+ cells and CD11b+ cells. Using an experimental model of viral myocarditis, they found that both CD103+ and CD11b+ cells – like DCs in other organs – are crucial for triggering an immune response to eliminate viruses infecting the heart.

The absence of these cells, especially CD103+ cells, not only suppressed the anti-virus response, but also led to significant heart damage that impaired the organ's pumping action, an early warning sign for heart failure.

Dr. Slava Epelman (Photo: UHN)

"Our findings suggest that CD103+ and CD11b+ DCs are required to prevent the progression of a mild infection to full blown heart failure by triggering an effective immune response to the virus," Dr. Epelman says.

This work was supported by the Canadian Institutes of Health Research, the Heart and Stroke Foundation, the March of Dimes Canada, the Ted Rogers Centre for Heart Research, the Heart & Stroke/Richard Lewar Centre of Excellence in Cardiovascular Research, the Peter Munk Cardiac Centre, the National Institutes of Health and the Toronto General & Western Hospital Foundation. M Cybulsky holds a Tier 1 Canada Research Chair in Arterial Wall Biology and Atherogenesis.

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