More on CCL17 as a Target to Reduce Inflammation in Cardiovascular Disease

Atherosclerosis is the buildup of fatty plaques in the walls of blood vessels, impeding blood flow and eventually rupturing to produce a heart attack or stroke. It is the single largest cause of human mortality. Atherosclerosis is in part an inflammatory condition, accelerated by the state of chronic inflammation that arises in later life. In this context, levels of CCL17 have been shown to rise with age, while inhibition of CCL17 has been shown to reduce chronic inflammation and slow the progression of atherosclerosis. This outcome is achieved via effects on T cell behavior; CCL17 is expressed on the surface of dendritic cells and interacts with CCR4 on the surface of T cells. In doing so it represses the anti-inflammatory activity of regulatory T cells. Researchers continue to investigate the biochemistry involved in this relationship. The authors of today's open access paper here report that CCR4 isn't the only receptor involved, and CCL17 also binds to CCR8. This sort of investigative work is necessary to understand how and where to target a specific mechanism. As researchers note, CCL17 does have a normal, useful role in coordinating transient immune activity where it is needed. As is the case for most age-related dysregulation of immune function, one can't just inhibit an overactive mechanism without consequences, as excessive immune activate uses the same pathways as normal immune activation. The aim of tracing the various interactions involved like this is to f...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs