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Statins, such as pravastatin, simvastatin, and lovastatin, are a highly successful class of cholesterol-lowering drugs that prevent heart attack by reducing the amount of unhealthy fat circulating in the blood. They achieve this by inhibiting the activity of a liver enzyme called 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Surprisingly, these drugs have also been shown to reduce atherosclerosis (artery narrowing) in heart transplant patients, by a mechanism that is independent of their action on cholesterol.
Now, a team at University Hospital Geneva, report for the first time that the statin drugs have an effect on the immune system (Nature Medicine, Vol. 6, Issue 12, 01 Dec 2000). François Mach and colleagues show that statins block the ability of a cytokine called interferon-gamma (IFN-gamma) to activate cells of the immune system called T-cells. Normally, IFN-gamma causes T-cells to express the Major Histocompatibility Complex class II (MHC-II) molecule that takes in foreign antigens and presents them on the surface of immune cells, thus propagating the inflammatory response. In discovering this mechanism, the scientists are able to explain why the drugs have potentially beneficial effects in a range of inflammatory diseases. The authors conclude, "This provides a firm scientific rationale to recommend the use of this drug as an immunosuppressor in organ transplantation." Wulf Palinski of the University of California, San Diego, discuss the findings and their clinical implications in an accompanying News & Views article. CONTACT: Dr François Mach
Cardiology Division,
Department of Medicine,
University Hospital Geneva,
Foundation for Medical Research,
64 Avenue Roseraie,
1211 Geneva 4,
Switzerland.
Tel: +41 22 382 7234
Fax: +41 22 347 5979
Email: machf@cmu.unige.ch Dr Wulf Palinski
Department of Medicine 0682
University of California San Diego
9500 Gilman Drive MTF 110
LaJolla, CA 92093
Tel: +1 858 534 7818
Email: wpalinski@ucsd.edu
(C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
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