Researchers gain better understanding of deadly autoimmune heart ailment that affects young adults

Researchers at the Johns Hopkins Bloomberg School of Public Health have discovered that complement, a key protein of the innate immune system, is critical to the development of autoimmune myocarditis. According to the study appearing in the August 2001 issue of Nature Immunology, the researchers prevented autoimmune myocarditis in mice by blocking the production of complement and by blocking its interaction with two key complement receptors. The study examines the role of the innate immune system during the formation of autoimmune myocarditis, which may lead to better diagnosis and prevention of this deadly disease and other autoimmune disorders.

Myocarditis is an inflammation of the heart muscle and is a principal cause of heart disease and sudden cardiac death in young adults. It is often caused by infection from a coxsackie virus. While most people recover from viral myocarditis with no ill effects, a small number of people develop autoimmune myocarditis in which the bodys own immune system attacks the heart muscle, eventually leading to heart failure.

We wanted to know why myocarditis triggers an autoimmune response in a small group of people. Our research shows that complement and its receptors are key pieces of that puzzle, says Noel R. Rose, MD, PhD, professor molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health and professor of pathology and medicine at the Johns Hopkins School of Medicine.

As Dr. Rose explains, the body has two levels of defense in the immune system: the innate immune response, which we are born with, and the adaptive immune response, which we learn by experience. The innate immune system "holds the fort" with complement, which motivates T-cells and cytokines of the adaptive immune system to mount a response and fight off the infection. It is during this learning phase, the researchers believe, that complement plays a critical role in the development of autoimmune myocarditis.

Contact: Tim Parsons or Ming Tai
Johns Hopkins University Bloomberg School of Public Health

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