Around 64 million people worldwide suffer from heart failure, and nearly half die within the first five years of diagnosis due to a lack of effective treatments to stop the disease from getting worse.

Heart failure occurs when the heart’s ability to pump blood drops to less than 40%. Most available treatments tend to focus on reducing the effort necessary for the heart to pump blood, rather than tackling the underlying causes of the disease. This is mostly because researchers still don’t know what causes heart failure and what makes it worsen with time.

Turns out the immune system, the body’s protection against infection and disease, may be responsible for worsening heart failure.

T cells heal and harm

For the past 13 years, I have been studying how the T cells of the immune system behave during heart failure.

T cells help the body heal from injuries and fight infections. They do this by making proteins called anti-inflammatory cytokines that help wounds close, and recruiting or modifying other immune cells that kill invading pathogens.

However, when T cells are mistakenly activated against the body’s own cells, it can cause autoimmune diseases. For example, Type 1 diabetes is caused by T cells attacking pancreatic cells, and psoriasis occurs when T cells are activated against skin cells.

T cells and heart failure

If T cells can help heal things like wounds on the skin, why are they unable to heal the heart? My team and I have been working to answer this question.

In initial studies in mice, we found that a type of immune cell called helper T cells makes proteins called pro-inflammatory cytokines that induce more damage to the heart during heart failure, making the disease worse.

In our latest research, we have been studying failing hearts obtained from patients receiving a transplant or an artificial pump. We found that T cells remain active in failing hearts and also turn on pro-inflammatory proteins that worsen heart damage instead of healing the heart.

We also found that the proteins within T cells of failing hearts are similar to proteins seen in T cells involved in autoimmune diseases. These parallels suggest that heart failure induces T cells to behave similarly to those in autoimmune disease rather than those that heal injuries.

Heart failure and autoimmunity

How T cells are activated in the heart might contribute to the worsening heart damage that results in slow and sustained disease progression.

While the underlying mechanisms behind heart failure remain elusive, our findings suggest that viewing heart failure as an autoimmune condition could help lead to new treatments.

Further research on how to stop T cells from damaging the heart could provide a way to stop heart failure from worsening and save the lives of millions of patients.

Shyam Bansal receives funding from the National Heart, Lung and Blood Institute of the National Institutes of Health, the American Heart Association and the W.W. Smith Charitable Trust. He is a member of the American Heart Association and the Society for South Asian Heart Research.