Medical Science

The Long Arm of the Dendritic Cell

A link between atherosclerosis and autoimmunity

20. 4. 2012 | Individuals who suffer from autoimmune diseases also display a tendency to develop atherosclerosis – the condition popularly known as hardening of the arteries. Researchers at the Rudolf-Virchow-Center in Würzburg, together with colleagues from the Ludwig Maximilians University in Munich (LMU), have now discovered a mechanism that helps explain the connection between the two types of disorders.
Atherosclerosis is a major cause of death in Western societies. The illness is induced by the formation of insoluble deposits called atherosclerotic plaques on the walls of major arteries as the consequence of chronic, localized inflammations. By reducing blood flow, the plaques can provoke heart attacks and strokes. A class of immune cells called dendritic cells plays a crucial role in facilitating the development of these plaques. Among these cell types are the so-called plasmacytoid dendritic cells (pDC), but their potential significance for atherosclerosis had not been systematically explored until now.

A group of researchers supervised by associate professor Dr. Alma Zernecke at Würzburg University, together with a team led by life scientist Dr. Yvonne Döring at LMU, has now shown how pDCs promote the development of atherosclerosis. "This could be the reason why patients with autoimmune diseases like psoriasis or systemic lupus erythematodes (SLE) develop atherosclerosis more frequently", Zernecke explains. "Indeed, both disorders feature overactive pDCs." pDCs respond to DNA released from damaged and dying cells by secreting interferon proteins which stimulate the immune reactions against some of the body's own proteins - a reaction typical for autoimmune diseases.
The new study shows that stimulation of pDCs by a specific DNA-protein contributes to the progression of atherosclerosis. The findings may entail new treatment strategies for an entire spectrum of conditions that are associated with chronic inflammatory reactions.

Using laboratory mice as an experimental model, the researchers were able to show that pDCs contribute to early steps in the formation of athersclerotic lesions in the blood vessels. Stimulation of pDCs causes them to secrete large amounts of interferons, proteins that strongly stimulate inflammatory processes. The protein that induces the release of interferons is produced by immune cells that accumulate specifically at sites of inflammation, and mice that are unable to produce this protein also have fewer plaques. Furthermore, stimulation of pDCs leads to an increase in the numbers of macrophages present in plaques. Macrophages normally act as a clean-up crew, removing cell debris and fatty deposits by ingesting them. However, they can also "overindulge", taking in more fat than they can digest. When this happens, they turn into so-called foam cells that promote rather than combat atherosclerosis.
According to this model, the stimulation of pDCs provides the link between atherosclerosis and autoimmune diseases.   (© Ludwig Maximilians University Munich)
Dr. Monika Gödde

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