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Two-way link between heart disease and autoimmunity

Autoimmune diseases such as rheumatoid arthritis and lupus are associated with an increased risk of atherosclerosis and heart disease, which is the leading cause of death in the developed world. A new mouse model, reported by Kenneth Walsh and colleagues in The Journal of Experimental Medicine, now shows that the converse is also true -- atherosclerosis can make autoimmunity worse.

Patients with autoimmune disease, in which the body's immune system attacks its own tissues, have higher levels of fatty deposits in blood vessels (known as atherosclerotic lesions), which cause heart disease. To investigate the link between these disorders, the authors crossed an autoimmune-prone mouse with another that develops atherosclerosis to create a new mouse strain with susceptibility to both diseases.

These mice had bigger fatty deposits in their blood vessels than the parent mice that were only susceptible to atherosclerosis. So, as in humans, autoimmune disease makes heart disease worse. This ties in with the proposed role of immune cells in forming atherosclerotic lesions.

The authors were surprised to find also that atherosclerosis worsens autoimmunity. The new mice had more severe autoimmune symptoms than the parent mice that were only susceptible to autoimmunity. Symptoms were made even worse by feeding the mice a high-fat diet, as is common in Western countries.

Autoimmune disease can be caused by inefficient removal of the dying cells that result from constant cell turnover in our bodies. If this cellular debris accumulates, it can trigger an immune response against our own organs. The new mice had high levels of such debris. Walsh and colleagues think that the oxidized fats that cause atherosclerosis also prevent the removal of dead-cell garbage and autoimmunity results.

This work implies that patients with autoimmune disease may benefit from low-fat diets.


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Contact: Nickey Henry
henryn@rockefeller.edu
212-327-8575
Journal of Experimental Medicine
19-Apr-2004


Page: 1

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