Researchers in Berlin, Germany have found that a specific type of immune cell, the regulatory T lymphocyte (Treg) plays an important role in hypertension-induced cardiac damage. The injected Treg that they harvested from donor mice into recipient mice were infused with angiotensin II, a blood pressure-raising peptide. The Tregs had no influence on the blood pressure response to angiotensin II. Nonetheless, cardiac enlargement, fibrosis, and inflammation was sharply reduced by Treg treatment. Furthermore, the tendency to develop abnormal heart rhythms that could lead to sudden cardiac death was also reduced. Dr. Heda Kvakan and Dr. Dominik N. Mller at the Experimental and Clinical Research Center at the Max Delbrck Center do not intend Treg as a therapy. However, a better understanding of how the immune system fits into hypertension-induced organ damage could result from these studies (Circulation, Vol. 119, No. 22, June 9, 2009, 2904-2912 ).*
The researchers transferred Treg cells into mice. These cells normally keep the immune system in balance. If the number of Treg cells is reduced or their function impaired, the immune system gets out of balance and, rather than recognizing and destroying bacteria or viruses, the immune cells attack body tissue or organs instead. Autoimmune diseases, such as diabetes type I or Multiple sclerosis, result from the malfunctioning of the immune system.
Aside from its physiological role in maintaining blood pressure, it has long been known that the hormone angiotensin II plays a pivotal role in the onset of hypertension and in subsequnt hypertensive organ damage, e.g. cardiac hypertrophy.
Angiotensin II also has proinflammatory properties and actives the cells of the immune system. The activation of these cells also seems to have a major part in Angiotension II-induced target organ damage. The researchers wanted to know if the suppression of activated immune cells by Treg cells could reduce ca
'/>"/>
| Contact: Barbara Bachtler bachtler@mdc-berlin.de 49-309-406-3896 Helmholtz Association of German Research Centres Source:Eurekalert |