The reason why the normally transient inflammatory response is not turned off and becomes chronic, secreting a signal molecule that promotes atherosclerosis has been revealed in a new study.
The persistence of the inflammatory reaction is due to a loss of control over the activity of the immune system. So-called dendritic cells are known to play a central role in the adaptive immune response, functioning as activators of other classes of immune cells.
Now, an international team of researchers led by Professor Christian Weber of Ludwig-Maximilians-University (LMU) Munich and Privatdozentin Alma Zernecke of Würzburg University has demonstrated that dendritic cells release the chemokine CCL17 as a signal molecule, which inhibits a feedback mechanism that normally limits the activity of the immune system.
The new study has also identified a potential antidote to the signal molecule. As Professor Weber reports, "We were able to prevent the progression of atherosclerosis using an antibody raised against CCL17."
In other words, CCL17 offers a promising starting point for the development of new therapeutic strategies.